















U * I 





















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Radiograph of a Healthy Child's Chest. 



PHYSICAL DIAGNOSIS 



OF 



DISEASES OF THE CHEST 



' y 

BY 



RICHARD C. CABOT, M.D. 

PHYSICIAN TO OUT-PATIENTS, MASSACHUSETTS GENERAL HOSPITAL; ASSISTANT IN 
CLINICAL MEDICINE, HARVARD MEDICAL SCHOOL 



WITH ONE HUNDRED AND 
FORTY-TWO ILLUSTRATIONS 



NEW YORK 

WILLIAM WOOD AND COMPANY 

MDCCCC 



B8774 



ji.ibrfe.iy of OonciiHSM 

OCT 31 1900 

Cap ytfght «try 

SECOND COPY. 

0<-i<v*«-«i to 

OWkH DIVISION, 

OCT 31 1900 



A' 



D 



Copyright, 1900, 
By WILLIAM WOOD AND COMPANY. 



PRESS OF PUBLISHERS' PRINTING COMPANY 
32, 34 LAFAYETTE PLACE, NEW YORK. 



FREDERICK C. SHATTUCK, M.D. 

Jackson Professor of Clinical Medicine 
in Harvard University 



IN EVIDENCE OF MY APPRECIATION OF 

THE EXAMPLE OF SINCERITY, COMMON SENSE, AND ENTHUSIASM 

ESTABLISHED BY HIM IN THE TEACHING AND 

THE PRACTICE OF MEDICINE 



PREFACE 



This book is intended for students and, so far as I am aware, 
contains nothing original. I have written it because I have not 
been able to find any small work upon the subject which does not 
contain glaring errors. The correct books are too large; the small 
books are out of date and repeat such well-worn myths as that the 
aortic second sound is normally louder than the pulmonic second, 
that aortic regurgitant murmurs are usually best heard in the sec- 
ond right interspace, that a hypertrophied left auricle can produce 
dulness and pulsation near the left sternal border, that systolic re- 
traction at the cardiac apex means adherent pericardium, that epi- 
gastric pulsation denotes hypertrophy of the right ventricle, etc. 
Further, none of the smaller text-books contains any adequate ac- 
count of muscle sounds, of pulmonary atelectasis, or of adherent 
pericardium. To record the well-known but often forgotten truth 
on such matters as these has seemed to me of importance in small 
books as well as in encyclopaedic treatises. 

The diagrams illustrating respiratory types are modifications of 
those used by Wylie and Sahli. 

I am indebted to Mr. Eliot Alden, of the Harvard Medical 
School, for his kind assistance in the preparation of the illustra- 
tions and to Drs. E. C. Bradford and R. W. Lovett for permission 
to use three cuts from their well-known work on orthopedic sur- 
gery. 

I am also indebted to the editor of the Archives of the Rontgen 
Ray for permission to use two radiographs from that journal. 



TABLE OF CONTENTS. 



Introduction, 

I. Methods of Examining the Thoracic Organs, . 
II. Regional Anatomy of the Chest, . 



PAGE 

, 1 

. 1 

, 2 



III. 



IV. 



PART I. 

TECHNIQUE AND GENERAL DIAGNOSIS. 

CHAPTER I. 

INSPECTION. 

Size, .... 

Shape, .... 

(a) The Rachitic Chest, 

(6) The Paralytic Chest, 

(c) The Barrel Chest, . 
Deformities, . 

(a) Curvature of the Spine, 

(6) Flattening of One Side of the Chest, 

(c) Prominence of One Side of the Chest 

(d) Local Prominences, . 
Respiratory Movements, 

(a) Normal Respiration, 

(6) Anomalies of Expansion, 

1. Diminished Expansion, 

2. Increased Expansion, 
(c) Dyspnoea, 

The Respiratory Rhythm, 
(a) Asthmatic Breathing, 
(6) Cheyne-Stokes Breathing, 

(c) Restrained Breathing, 

(d) Shallow and Irregular Breathing. 

(e) Stridulous Breathing, 



12 
12 
14 
14 
15 
16 
10 
16 
17 
18 
18 
21 
21 
21 
22 
22 
28 



vm TABLE OF CONTENTS. 

PAGE 

VI. Diaphragmatic Movements (Litten's Phenomenon), . . .23 
VII. The Cardiac Movements, . 26 

1. Normal Cardiac Impulse, . 26 

2. Displacement of the Cardiac Impulse, 29 

3. Apex Retraction, .... .... 31 

4. Epigastric Pulsation, . . . ... . . .32 

5. Uncovering of the Heart, 32 

VIII. Aneurism and Other Causes of Abnormal Pulsations or the 

Chest Wall, 33 

IX. The Peripheral Vessels, 34 

(a) Venous Phenomena, . . 35 

(b) Arterial Phenomena, . .36 

(c) Capillary Phenomena, ........ 38 

X. The Skin and Mucous Membranes, ...... 39 

1. Cyanosis, 39 

2. (Edema, 40 

3. Pallor, 40 

4. Jaundice, . . . . . .40 

5. Scars and Eruptions, 41 

XI. Enlarged Glands, . 41 



CHAPTER II. 
PALPATION AND THE STUDY OF THE PULSE. 

I. Palpation, ............ 42 

1. The Cardiac Impulse, . . . . . . . . .42 

2. Thrills, . . . ... . . . . . .43 

3. Tactile Fremitus, 44 

4. Friction, Pleural or Pericardial, . . . . . . .46 

5. Palpable Rales, ' . . . . .47 

6. Tender Points, 48 

7. Abnormal Pulsations . 48 

8. Tumors, 48 

9. Temperature and Quality of the Skin, 49 

II. The Pulse, . 49 

1. The Rate, 51 

2. Rhythm, 51 

3. Compressibility, 52 

4. Size and Shape of Pulse Wave, 52 

5. Tension, 53 

6. Size and Position of Artery, 55 

7. Condition of Artery Walls, 55 



TABLE OF CONTENTS. 
CHAPTER III. 



IX 



PERCUSSION. 



I. Technique, 

^ Mediate Percussion, .... 
' a ' } Immediate Percussion, 

(b) Auscultatory Percussion, . . . 

(c) Palpatory Percussion, .... 

II. Percussion-Resonance of the Normal Chest 
(a) Vesicular Resonance, .... 
(6) Dulriess and Flatness, .... 

(c) Tympanitic Resonance, 

(d) Cracked-pot Resonance, 

(e) Amphoric Resonance. . 
(/) The Lung Reflex, . 

III. Sense of Resistance, .... 



PAGE 

. 58 
. 58 
. 58 
. 65 
. 67 
. 67 
. 68 
. 68 
. 70 
. 74 
. 75 
. 76 
. 76 



CHAPTER IV. 

AUSCULTATION. 

1. Mediate and Immediate Auscultation, . . „ . 77 

2. Selection of a Stethoscope, ........ . . . „• 7.8 

3. The Use of the Stethoscope, ......... 83 

A. Selective Attention and What to Disregard, . „ „ .84 

B. Muscle Sounds, . . . .86 

C. Other Sources of Error, ...... „ . . 88 

4. Auscultation of the Lungs, . . . . . . .91 

I. Respiratory Types, . 92 

(a) Vesicular Breathing, ...... . . 93 

(6) Tubular Breathing, ......... 95 

(c) Broncho-vesicular Breathing, ...... 96 

(d) Emphysematous Breathing, . 97 

(e) Asthmatic Breathing, 97 

(/) Cog-wheel Breathing, 98 

(g) Amphoric Breathing, 98 

(h) Metamorphosing Breathing, 98 

II. Differences between the Right and the Left Chest, . . .99 

III. Pathological Modifications of Vesicular Breathing, . . . 99 

(a) Exaggerated Vesicular Breathing, ..... 99 
(6) Diminished Vesicular Breathing, ..... 100 

IV. Bronchial Breathing in Disease, ....... 102 



: TABLE OF CONTENTS, 

PAGE 

V. Amphoric Breathing, 103 

VI. Rales, 103 

(a) Moist, . . . . . . . . . . .103 

(6) Dry, 104 

(c) Musical, 106 

VII. Cough. Effects on Respiratory Sounds, 107 

VIII. Pleural Friction, . ......... 107 

IX. Auscultation of the Voice Sound, . 109 

(a) The Whispered Voice, 109 

(6) The Spoken Voice, . 110 

(c) Egophony, Ill 

X. Phenomena Peculiar to Pneumo-Hydrothorax, .... Ill 
(a) Succussion, . . . . . . . . . Ill 

(6) Metallic- Tinkle, 112 

(c) The Lung Fistula Sound, 112 



CHAPTER V. 

AUSCULTATION OF THE HEART. 

1. The Valve Areas, 113 

2. Normal Heart Sounds, ..... .... 114 

3. Modifications in the Intensity of the Heart Sounds, . . . 116 

(a) Mitral First Sound, .117 

1. Shortening, . . ... . . • . . 117 

2. Doubling, 118 

(6) The Second Sounds at the Base of the Heart, . . . .118 

1. Physiological Variations, . 118 

2. Pathological Variations, . , 120 

(a) Accentuation of Pulmonic Second Sound, . . . 120 

(6) Weakening of Pulmonic Second Sound, . . . 121 

(c) Accentuation of the Aortic Second Sound, . . . 121 

(d) Weakening of the Aortic Second Sound, . . . 121 

(e) Accentuation of Both Second Sounds, .... 122 
(/) Summary, 122 

(c) Modifications in Rhythm of Cardiac Sounds and Doubling of Sec- 

ond Sounds 123 

(d) Metallic Quality of the Heart Sounds, 124 

(e) " Muffled " Heart Sounds, 124 

4. Sounds Audible Over the Peripheral Vessels, .... 124 

(a) Arterial Sounds, 124 

(6) Venous Sounds, .......... 125 



TABLE OF CONTENTS. 



XI 



CHAPTER VI. 

(Auscultation of the Heart Continued.) 

CARDIAC MURMURS. 

PAGE 

I. Terminology, . 126 

1. Mode of Production, .'.''.. 126 

2. Place of Murmurs in the Cardiac Cycle, ..'.'.. 128 

3. Point of Maximum Intensity, . . . . . . . 129 

4. Area of Transmission, 130 

5. Effects of Respiration, Exertion, and Position, . . . . 135 

6. Intensity, Quality, and Length, ...... 132-135 

7. Relation to Heart Sounds,. ....... 135 

8. Metamorphosis of Murmurs, ....... 136 

II. Functional Murmurs, . . . . . . . . .136 

III. Cardiorespiratory Murmurs, 138 

IV. Venous Murmurs, .......... 139 

V. Arterial Murmurs, 140 



PAET II. 



DISEASES OF THE HEAET. 
CHAPTER VII. 



VALVULAR LESIONS. 

1. Valvular and Parietal Disease, 

2. The Establishment and Failure of Compensation. 

3. Hypertrophy and Dilatation, . 

4. Valvular Disease, 

I. Mitral Regurgitation, 

(a) Pre-compensatory Stage, 
(&) Stage of Compensation, . 

(c) Stage of Failing Compensation, 

(d) Differential Diagnosis, . 
II. Mitral Stenosis, 

1. First Stage, 

2. Second Stage, . 

3. Third Stage, . 

4. Differential Diagnosis, . 
III. Aortic Regurgitation, 

1. Inspection, 



. 


141 


o 


144 


. o 


146 


. 


151 


. c 


151 





153 


. . . 


154 


. . 


158 


. 


159 


. 


161 


. 


163 


. 


165 





166 





107 




170 


. . . 


171 



xii TABLE OF CONTENTS. 

PAGE 

(a) Arterial Jerking, . ....... 172 

(6) Capillary Pulsation, ....... 173 

2. Palpation, 174 

3. Percussion, 175 

4. Auscultation, 175 

5. Summary and Differential Diagnosis, , . . . . 178 

6. Prognosis, . . . . . . . . . - . 179 

7. Complications, 179 

IV. Aortic Stenosis, . . 180 

1. (a) The Murmur, 181 

(6) The Pulse, 183 

(c) The Thrill, 184 

(d) Feeble Aortic Second Sound 184 

2. Differential Diagnosis, 184 

V. Tricuspid Regurgitation, 187 

1. (a) The Murmur, 188 

(6) Venous Pulsation, . 188 

(c) Cardiac Dilatation, 189 

(d) Feeble Pulmonic Second Sound, ..... 189 

2. Differential Diagnosis, . . . „ . . . .190 
VI. Tricuspid Stenosis, 191 

VII. Pulmonary Regurgitation, ... . . . . . 192 

VIII. Pulmonary Stenosis, . .193 

IX. Combined Valvular Lesions, 194 

(a) Double Mitral Disease, . . . o . . . . 195 

(6) Aortic and Mitral Regurgitation, ...... 196 

(c) Aortic Stenosis and Regurgitation, . . . . . 197 

CHAPTER VIIL 

PARIETAL DISEASE AND CARDIAC NEUROSES. 

I. Acute Myocarditis, . 198 

1. Acute Moycarditis, 198 

2. Chronic Myocarditis, 199 

3. Fatty Overgrowth, 201 

4. Fatty Degeneration, . . . 201 

II. Cardiac Neuroses, . . . . . . . . . . 202 

1. Tachycardia, 202 

2. Bradycardia, 203 

3. Arrhythmia, 204 

4. Palpitation, 205 

5. Congenital Heart Disease, 206 



TABLE OF CONTENTS. 



xm 



CHAPTER IX. 
DISEASES OF THE PERICARDIUM. 

PAGE 

I. Pericarditis, 209 

(a) Dry or Fibrinous, 209 

(b) Pericardial Effusion, . 212 

1. The Area of Dulness, 213 

2. The Cardiac Impulse and the Pulse, 214 

3. Pressure Signs, . . .215 

(c) Adherent Pericardium, 216 

1. Retraction of Interspaces, 217 

2. Limitation of Respiratory Movements, . . . .217 

3. Absence of Cardiac Displacement with Change of Position, 217 

4. Hypertrophy and Dilatation not otherwise Explained, . 217 

5. Capsular Cirrhosis of the Liver, . . . . . 218 
II. Htdropericardium and Pneumopericardium, ...... 219 

CHAPTER X. 

THORACIC ANEURISM. 

. 220 

. 221 

. 222 

. 222 

. 223 

. 224 

. 224 

. 225 

. 225 

. 226 

. 227 

. 227 

. 229 



1. 


Abnormal Pulsation, . 


2. 


Tumor, 


3. 


Thrill, .... 


4. 


Diastolic Shock, . 


5. 


Tracheal Tug, 


6. 


Pressure Signs, 


7. 


Percussion Dulness, 


8. 


Auscultation, 




(a) Murmurs, 




(6) Diastolic Shock Sound 


9. 


Radioscopy, . 


10. 


Summary, 


11. 


Diagnosis, . 



PART III. 

DISEASES OF THE LUNGS AND PLEURA. 

CHAPTER XL 
BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 



1. Tracheitis, 

2. Bronchitis, 



. 283 
. 233 



xiv TABLE OF CONTENTS. 

PAGE 

(a) Physical Signs, . -234 

(6) Differential Diagnosis, . . . . ... 235 

3. Croupous Pneumonia, 237 

(a) Inspection, 237 

(6) Palpation, . . . 238 

(c) Percussion, 238 

(d) Auscultation, 239 

(e) Summary, . . . . - 242 

(/) Differential Diagnosis, 242 

4. Broncho-Pneumonia, .......... 244 

5. Pulmonary Tuberculosis, 245 

(a) Incipient Tuberculosis, 245 

(6) Moderately Advanced Cases, ....... 249 

(c) Advanced Phthisis, 252 

(d) Anomalous Forms of Pulmonary Tuberculosis, . . . . 256 



CHAPTER XII. 

(Diseases of the Lungs, Continued.) 

1. Emphysema, 258 

(a) Small-Lunged Emphysema, 258 

(6) Large-Lunged Emphysema, 258 

(c) Emphysema with Bronchitis and Asthma, ..... 261 

(d) Interstitial Emphysema, ........ 262 

(e) Complementary Emphysema, 262 

(/) Acute Pulmonary Tympanites, ....... 262 

2. Bronchial Asthma, .......... 263 

3. Syphilis of the Lung, . . . . . . . . . 264 

4. Bronchiectasis, 264 

5. Cirrhosis of the Lung, 265 



CHAPTER XIII. 

DISEASES AFFECTING THE PLEURAL CAVITY. 

I. Hydrothorax, 266 

II. Pneumothorax, 266 

III. Pneumohydrothorax and Pneumopyothorax, 268 

Differential Diagnosis of Pneumothorax and Pneumohydrothorax, . 270 

IV. Pleurisy, 271 

1. Dry Pleurisy, , 271 



TABLE OF CONTENTS. 



xv 



Pleuritic Effusion, 

(a) Percussion, .... 

(b) Auscultation, 

(c) Inspection and Palpation, . 
Pleural Thickening, 
Encapsulated Pleural Effusions, . 
Pulsating Pleurisy and Empyema Necessitatis, 
Differential Diagnosis of Pleural Effusions, 



PAGE 

. 273 
. 273 
. 279 
. 281 
. 283 
. 283 
. 284 
. 284 



CHAPTER XIV. 

ABSCESS, GANGRENE AND CANCER OF THE LUNG, PULMONARY 
ATELECTASIS, CEDEMA AND HYPOSTATIC CONGESTION. 

1. Abscess and Gangrene of the Lung, 290 

2. Cancer of the Lung, 291 

3. Atelectasis, . .292 

4. Oedema and Hypostatic Congestion, .,..*.. 293 



APPENDICES. 

Appendix A. — Diseases of the Mediastinum, 

1. Mediastinal Tumors, .... 

2. Mediastinitis, 

3. Tuberculosis of Mediastinal Glands, . 
Appendix B. — Acute Endocarditis, 
Appendix C. — Examination of Infant's Chests, 
Appendix D. — Radioscopy of the Chest, 
Appendix E. — The Sphygmograph, . 



293 
293 
295 

296 
296 
297 
298 
305 






PHYSICAL DIAGNOSIS 



OF 



DISEASES OF THE CHEST. 



INTRODUCTION. 

I. Methods of Examining the Thoracic Organs. 

To cany out a thorough examination of the chest we do five 
things: 1. We look at it; technically called " inspection." 2. We 
feel of it; technically called "palpation." 3. We listen to the 
sounds produced by striking it; technically called "percussion." 
4. We listen to the sounds produced within it by physiological or 
pathological processes; technically called "auscultation." 5. We 
study pictures thrown on the fluoroscopic screen or on a photo- 
graphic plate by the Roentgen rays as they traverse the chest; 
technically called "radioscopy." 

Measuring the dimensions or the movements of the chest ("men- 
suration ") is often mentioned as co-ordinate with the above meth- 
ods, but it yields very little information of practical value, and is 
at present very little used. 

The data obtained by examining the sputa, blood, and urine are 
frequently of great value in helping us to interpret the signs re- 
vealed by examination of the chest, but do not fall within the 
scope of this book. Accordingly, I shall confine myself in the 
first part of this book to a description of the methods of inspect- 
ing, palpating, percussing, and auscultating the chest, with a brief 
account of the physical signs which we have learned to appreciate 
by the use of these methods. (For radioscopy, see Appendix.) 
1 



PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



Without some knowledge of the regional anatomy of the chest 
no intelligent investigation of the condition of the thoracic organs 
can be carried on. Accordingly, I shall begin by recalling very 
briefly some of the most essential anatomical relations. 

II. Eegioxal Axatomy of the Chest. 

It seems to me a mistake to divide the chest into arbitrary por- 
tions and to describe physical signs with reference to such division. 
The seat of any lesion can best be described 
by giving its relation to the clavicle, ster- 
num, or ribs on the front and sides of the 
chest, and to the scapulae and ribs behind. 
Thus we may speak of rales as heard " above 
the left clavicle in front, " " below the right 
scapula behind, " " between the seventh and 
ninth ribs in the axilla," and so on. When 
we want to state more exactly what part of 
the axilla anteroposteriorly is affected, we 
may refer to the " mid-axillary line " (see 
Fig. 1) ; or better, we may place the lesion 
by measuring the number of centimetres or 
inches from the median line of the sternum. 
In a similar way the place of the apex im- 
pulse of the heart (whether in the normal 
situation or farther toward the axilla) can be 
determined by measuring from the median 
line of the sternum. Measurements refer- 
ring to the nipple are entirely useless in 
women and not very reliable in men. It is 
better to measure as above. 

If, then, we confine ourselves chiefly to 
the bones of the chest as landmarks, and 
fix, with reference to them, the position of any portion of the in- 
ternal organs which we desire to study, it becomes unnecessary to 
memorize any technical terms or to learn the position of any arbi- 
trary lines and divisions such as are frequently forced upon the 




FIG. l. 



The Mid- Axillary 
Line. 



INTRODUCTION. 3 

student. The only points which it is necessary to memorize once 
for all are : 

1. The position of the heart, lungs, liver, and spleen with ref- 
erence to the bones of the chest. 

2. The position of certain points which experience has taught 
us have a certain value in physical diagnosis. I mean (a) the 
so-called "valve areas" of the heart, which do not correspond to 
the actual position of the valves, for reasons to be explained later 



Upper lobe of left 
lung. 



Right lung 
Right auricle. — 

Liver. 




Left ventricle. 



Lower lobe of left 

lung. 



" Stomach. 



Fig. 2.— Position of the Heart, Lungs, Liver, and Stomach. The dotted lines correspond to the 
outlines of the lung ; the heavy continuous line represents the heart ; while the position of 
the liver and of the lower border of the stomach is indicated by light continuous lines. The 
ribs are numbered. 



on, and (b) the percussion outlines of the heart, liver, and spleen. 
These outlines do not correspond in size with the actual dimensions 
of the organs within, yet there is a definite relation between the two 
which remains relatively constant, so that we can infer the size of 
the organ itself from the outlines which we determine by percus- 
sion. The position of the organs themselves is shown in Figs. 2, 
3, and 4. It will be noticed in Fig. 2 that the lungs extend up 
above the clavicles and overlap the liver and the heart — facts of 
considerable importance in the physical examination of these or- 
gans, as will be later seen. It is also to be noticed how small 



4 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

a portion of the stomach is directly accessible to physical examina- 
tion, the larger part of it lying behind the ribs and covered by the 




Upper lobe. 



Lower lobe. 



Spleen. 

Lower lobe. 




Upper 
lobe. 



Middle 
lobe. 



Liver 



Fig. 3.— Position of the Left Lung from the F.'u. 4.— Position of the Right Lung from the 
Sides and of the Spleen. Side, and of the Liver. 

liver. The normal pancreas and kidneys are practically inacces- 
sible to physical examination. 

The percussion outlines — corresponding to those portions of 
the heart, liver, and spleen which lie immediately beneath the 
chest walls — will be illustrated in the section on Percussion (see 
page 58). 



PART I. 

TECHNIQUE AND GENERAL DIAGNOSIS. 



INSPECTION. 



Much may be learned by a careful inspection of all parts of the 
chest, but only in case the clothes are wholly removed. A good 
light is essential, and this does not always mean a direct light ; for 
example, when examining the front of the chest it is often better 
to have the patient stand with his side to the window so that the 
light strikes obliquely across the chest, accenting every depression 
and making every pulsation a moving shadow. In searching for 
abnormal pulsations, this oblique light is especially important. 

In examining the thorax we look for the following points : 

1. The size. . 

2. The general shape and nutrition. 

3. Local deformities or tumors. 

4. The respiratory movements of the chest walls. 

5. The respiratory movements of the diaphragm. 

6. The normal cardiac movements. 

7. Abnormal pulsations (arterial, venous, or capillary). 

8. The peripheral vessels. 

9. The color and condition of the skin and mucous membranes. 

10. The presence or absence of glandular enlargement. 

I. Size. 

Small chests are seen in patients who have been long in bed 
from whatever cause ; also in those who have suffered in infancy 
from rickets, adenoid growths in the naso-pharynx, or a combina- 
tion of the two diseases. Abnormally large chests are seen chiefly 
in emphysema. Of course the chests of healthy individuals vary 



6 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

a great deal in size at any given age, and I have been referring in 
the last sentences only to variations greater than those normally 
fonnd. 

II. Shape. 

There are marked differences in shape between the child's and 
the adult's chest in health. A child's trunk, as compared with 




Fig. 5.— Funnel Breast. 

that of an adult, is far more nearly cylindrical ; that is, the antero- 
posterior diameter is nearly as great as the lateral. The adult's 
chest is distinctly flattened from before backward, although indi- 
vidual variations in this respect are considerable, as Woods Hutch- 
inson has shown. 

In childhood the commonest pathological modifications are due 



INSPECTION. 7 

to rickets ; in middle and later life to emphysema, phthisis, or old 
pleuritic disease. 

(a) The Rachitic Chest. 

The sternum generally projects {"pigeon breast "), but in some 
cases, especially when rickets is combined with adenoid hyper- 
trophy, there may be a depression at the root of the sternum re- 
sulting in the condition known as "funnel breast " l (Figs. 5 and 6). 




Fig. 6.— Funnel Breast. 

The sides of the chest are compressed laterally and slope in to meet 
the sternum as the sides of a ship slope down to meet the keel 
(pectus carinatum) (Figs. 8, 9 and 10). From the origin of the ensi- 
form cartilage a depression or groove is to be seen running down- 
ward and outward to the axilla and corresponding nearly to the 
attachment of the diaphragm. This is sometimes spoken of as 
" Harrison' s groove " (Figs. 11 and 12). The lower margin of the ribs 

1 In some cases this condition appears to be congenital. 



8 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

in front often flares out, owing to the enlargement of the liver and 
spleen below and the pull of the diaphragm above. Along the line 
of the chondro-costal articulation there is to be felt, 'and sometimes 




Fig. 7.— Acquired Depression at the Root of the Ensiforin Cartilage. The patient is a shoe- 
maker of seventy, who has all his life pressed against his breast bone the shoe on which 
he worked. 

seen, a line of eminences or swellings, to which the name of "ra- 
chitic rosary " has been given (see Fig. 13). 

(b) The "Paralytic Thorax." 

Fig. 14 conveys a better idea of this form of chest than any 
description. The normal anteroposterior flattening is exaggerated 
so that such persons are often spoken of as "flat-chested." The 
clavicles are very prominent, owing to falling in of the tissues 



IXSPECTION. 9 

above and below them; the shoulders are stooping, the scapulae 
prominent, and the neck is generally long. The angle where the 
ribs meet at the ensif orm cartilage, the so-called " costal angle, " is in 
such cases very sharp. This type of chest has often been supposed 
to be characteristic of phthisis, but may be found in persons with 
perfectly healthy lungs. On the other hand, phthisis frequently 




fig. 



-Pigeon Breast. 



exists in persons with normally shaped chests or with abnormally 
deep chests (Woods Hutchinson). (See Fig. 128, page 251.) 



(c) The "Barrel Chest." 

Nothing is less like a barrel than the "barrel chest." Its most 
striking characteristic is its greatly increased anteroposterior diam- 
eter, so that it approaches the form of the infant's chest. The 
costal angle is very obtuse, the shoulders are high, and the neck 
is short. The respiratory movements of the barrel chest will be 
spoken of later (see Figs. 15 and 16). 



10 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Nutrition of the Chest Walls. 

Emaciation is readily appreciated by inspection. The ribs are 
unusually prominent, the scapulae stand out, and the clavicles pro- 
ject. All this may be seen independently of any change in the 




Fig. 9.— Pigeon Breast. 



shape of the chest such as was described above under the title of 
Paralytic Thorax. Tuberculosis of the apices of the lungs may 
produce a marked falling in of the tissues above and below the 
clavicle independent of any emaciation of the chest itself. 



INSPECTION. 



11 




Fig. 10.— Pigeon Breast. 



12 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

III. Deformities. 

The abnormalities just enumerated are symmetrical and affect 
the whole thorax. Under the head of Deformities, I shall consider 
chiefly such abnormalities as affect particular portions of the chest 
and not the thorax as a whole. 

(") Spinal Curvatures and Twists. 

A good view of the patient's back brings out best the lesser de- 
grees of lateral curvature, which are not at all infrequent in persons 




Fig. 11.— Harrison 1 s Groove. 

who are not aware of them. Slight degrees of deformity are best 
seen by marking with a skin-pencil the position of the spinous proc- 
esses (see Fig. 18). The more marked cases of lateral curvature, 
which are usually accompanied by a certain amount of twisting, 
give rise to considerable displacement of the thoracic organs and 
render unreliable the usual bony landmarks, with reference to 
which we judge of the position of the intrathoracic organs. By 
such deformities the apex of the heart may be pushed up into the 



INSPECTION. 



13 




Fig. 12.— Harrison's Groove. 

fourth space or out into the axilla, or portions of the lungs may 
be compressed and made atelectatic. 

I. The bulging on the convex side of the curve may simulate 
an aneurismal tumor. 

II. Pott's disease of the spine should be looked for as a part 




Fig. 13.— Remains of Rachitic Rosary in a Boy of Seventeen. 



14 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



of the routine inspection of the chest. It is sometimes better felt 

than seen. 

III. Abnormal rigidity of the spine, clue to spondylitis defor- 
mans, is to be recognized by watching the movements of the spinal 
column as the patient bends forward and back.^ Where the verte- 
brae are locked together, as occurs in moderately advanced cases of 

this disease, the spine is 
maintained rigidly stiff, in- 
dependent of muscular sup- 
port. A similar stiffness of 
the spine may also be seen 
in early Pott's disease. It 
is here due mostly to mus- 
cular spasm. 

(b) Flattening of One Side 
of the Chest. 

In chronic phthisis, cir- 
rhosis of the lung, or long- 
standing pleuritic effusion, 
marked falling in of one 
side of the chest is often to 
be seen. This may be ap- 
parent in the upper and 
front portion, beneath the 
Fig. 14.— The Paralytic Thorax. clavicle, or in the axilla, Or 

iii both situations (see Figs. 
14 and 20). The shrinkage of the affected side is made more ob- 
vious by contrast with the compensatory hypertrophy of the sound 
lung, which makes the sound side unusually full and prominent. 




(c) Prominence of One Side of the Chest. 

In pneumothorax or pleural effusions, and sometimes in malig- 
nant disease of the lung or pleura, there is a marked increase in the 
size of the affected side of the chest. Very rarely emphysema 



INSPECTION. 



15 



may affect one lung predominantly. In pneumothorax or pleuritic 

effusion we usually see, in addition to the above enlargement of the 

affected side, a smoothing out of 

the intercostal depressions so that 

the surface of that side is much 

more uniform than the other side. 

Bulging of the interspaces from 

great pressure within the chest is 

said to occur. I have never seen 

it and am somewhat sceptical as 

to its occurrence. 

(d) Local Prominences. 

In nearly one-quarter of all 
healthy chests that part of the 
thoracic wall which overlies the 
heart (the so-called "precordial 
region ") is abnormally promi- 
nent. The cause of this condi- 
tion is much disputed. A similar 
prominence may be brought about 
in children, whose thoracic bones 
are very flexible (and occasionally 
in older patients), by the outward 
pressure of an enlarged heart or 
of an effusion in the pericardial 
sac. The prominences due to 
spinal curvature have been al- 
ready mentioned. Less common 
causes of local prominence are : 

1. Aneurism of the arch of 
the aorta. 

2. Tumor of the chest wall 

(lipoma, sarcoma, gumma) or of the lung, mediastinum, or of the 
thoracic glands pressing their way outward. 




Fig. 15.— Barrel Chest in a Case of Bron- 
chial Asthma (eet. 13). 



16 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

3. " Cold abscess " (tuberculosis) of a rib or of the sternum. 

4. Empyema perforating the chest wall, the so-called " empyema 
necessitatis." 

IV. The Eespiratory Movements. 



(a) Normal Respiration. 

During normal respiration, one sees the ribs move outward and 
upward with inspiration, and downward and inward with expira- 
tion. Possibly one catches some 
hint of the movements of the 
diaphragm at the epigastrium. 
In men, diaphragmatic breath- 
ing is more marked, while in 
women breathing is mostly of 
the " costal type " ; that is, is 
done by the intercostal muscles. 
In certain diseases an exaggera- 
tion of the costal or of the dia- 
phragmatic type of breathing 
may be seen. In emphysema, 
for example, and in some cases 
of asthma, the ribs move very 
little, and most of the work of 
respiration is performed by the 
diaphragm, whose pull upon the 
lower ribs can sometimes be distinctly seen during inspiration. On 
the other hand, when the movements of the diaphragm are impeded 
by the presence of fluid or a solid tumor, as in cirrhosis of the 
liver or leukaemia, the breathing has largely to be performed by the 
ribs, and becomes, as we say, costal in type (see below, p. 19). 




Fig. 16.— Barrel Chest. Chronic bronchitis 
and emphysema. 



[b) Anomalies of Expansion. 

If we watch the patient while he takes a full breath, we may 
notice certain variations from the normal type of respiratory move- 



INSPECTION. 



17 



ments. We may see : (1) Diminished expansion of one side (as a 
whole, or at the apex). (2) Increased expansion of one side. 

(1) If diminished expansion of one side is due to pleuritic effusion, 
pneumothorax, or solid tumor of the lung or pleura, the affected 
side is usually distended as well as immobile. When, on the other 




Fig. 17.— Severe Lateral Curvature (Un- 
treated) . 



Fig. 18.— Lateral Curvature Three Weeks 
After Correction. 



hand, the lung is retracted or bound down by adhesions, as in 
phthisis, old pleurisy, occlusion of the bronchus, or from the pres- 
sure of an aneurism, we have immobility combined with a retraction 
of the affected side. In tuberculous disease at the apex of the 
lungs, we may see one side or both sides fail to expand at the top. 
Restriction of the motion of one side of the chest may also be due 



18 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



to pressure from below the diaphragm. An enlarged liver or spleen 
and tumors of the hepatic or splenic region may in this way prevent 
the normal expansion of one or the other side of the thorax. Oc- 
casionally a hemiplegia or a unilat- 
eral paralysis of the diaphragm 
results in diminished movement of 
one side of the chest. 

(2) Increased expansion of one 
side of the chest is observed princi- 
pally as a compensatory or vicarious 
overfunctionmg of that side when 
the other side of the chest is thrown 
out of use by a large pleuritic effu- 
sion, by pneumothorax, long-stand- 
ing pleurisy with contraction, or 
other causes. 

(c) Dyspnosa. 

This term is often used rather 
loosely to include: (1) Difficult 
breathing, whether rapid or slow. 
(2) Unusually deep breathing, 
whether difficult or not. (3) Eapid 
breathing. 

True dyspnoea or difficult breath- 
ing is almost always rapid as well, 
and does not differ at all from the 
well-known phenomenon of being " out of breath " after a hard run 
or any violent exertion. Conceive these conditions as persisting 
over hours or days, and we have the phenomenon known as dysp- 
noea. The breathing is not only thick but labored; that is, per- 
formed with difficulty, and unusual muscles, not ordinarily called 
upon for respiration, come into play and are seen working above 
the clavicle and elsewhere. More or less distress is generally ex- 
pressed in the face, and there is often a blueness of the lips or a 
dusky color throughout the face. The commonest causes of dysp- 




FiG. 19.— Lateral Curvature Before Cor 
rection. 



INSPECTION. 



19 



noea are the various forms of heart disease, pneumonia, large 
pleuritic effusion, emphysema, asthma, and phthisis. 

Dyspnoea may affect especially inspiration, as, for example, 
when a foreign body lodges in the larynx, or in ordinary "croup." 
In such cases we speak of " inspiratory dyspnoea" distinguishing it 
from u expiratory dyspnoea" such as occurs in asthma and emphy- 
sema. In the latter condition the breath seems to enter the chest 
readily, but the difficulty is to get it out again. Expiration is 
greatly prolonged and often noisy. 

Combined types also occur in which both respiratory acts are 
difficult. 

Abnormally deep and full respiration, without any appearance of 
difficulty in the process, is sometimes seen near the fatal termina- 
tion of cases of diabetes, 
the so - called diabetic 
dyspnoea. 

Simple rapidity of 
breathing should be dis- 
tinguished from dyspnoea 
of any type. In adults 
the normal rate of respi- 
ration is about 22 per 
minute. In children, it is 
considerably quicker and 
more irregular. It is not 
desirable to attempt here 
to enumerate all the 
causes which may lead to 
a quickening of the respi- 
ration. Among the com- 
moner are muscular exer- fig. 20.-Contraction of Left Chest. Empyema, 
tion, emotional disturb- 
ance, diseases of the heart and lungs, and fluid or solid accumula- 
tions below the diaphragm, which push up that muscle and cause it 
to encroach abnormally upon the thoracic cavity. Most of the in- 
fectious fevers are also apt to be accompanied by quickened breath- 




20 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



ing, especially but not exclusively when the fever is associated with 
a disease of the heart, lung, pleura, or pericardium. 

Sucking-in of the interspaces in the lower axillary regions or 

below the clavicles may 
be seen in connection 
with dyspnoea when- 
ever the lungs are pre- 
vented by some cause 
from properly expand- 
ing during inspiration. 
Negative pressure i s 
thus produced within 
the chest, and the at- 
mospheric pressure 
without pushes in the 
more elastic parts of 
the thorax. This phe- 
nomenon is seen in col- 
lapse or atelectasis of 
a portion or the whole 
of a lung, such as may 
occur in obstruction at 
the glottis (in which 
case both sides are 
equally retracted) o r 
from occlusion of a 
bronchus. In the lat- 
ter event, the sucking-in of the interspaces during inspiration oc- 
curs only on the affected side. 1 

1 Slight retraction of the lower interspaces in the axilla during inspiration 
is often seen in health. In disease this phenomenon is greatly exaggerated. 




Fig. 21.— Prominence of Right Side. Pleural Effusion. 



INSPECTION. 21 

V. Changes in the Respiratory Rhythm. 

(a) Asthmatic Breathing. 

In asthma the normal rhythm is reversed and the expiration 
becomes longer, instead of shorter, than inspiration. Inspiration 
may be represented only by a short gasp, while expiration becomes 
a prolonged wheeze lasting several times as long as inspiration. 
Dyspnoea is usually very marked. In emphysema we get very 
much the same type of breathing so far as rhythm is concerned, 
but the dyspnoea is not usually so extreme and the auxiliary mus- 
cles of respiration are not so apt to be called into use. In many 
cases of emphysema one sees the thorax move all as one piece, " en 
cuirasse," owing to a senile fixation of the bones of the thorax from 
ossification of the cartilaginous portions. In hereditary syphilis 
this fixation may occur in youth or early middle age. 

(b) C hey ne- Stokes Breathing. 

An anomaly of respiratory rhythm in which short, recurrent 
paroxysms of dyspnoea are preceded and followed by periods in 
which no respiration occurs (apnoea). If we represent the normal 
respiratory movement by an up-and-down line, as seen in Fig. 22, 

vwvwww 

Fig. 33.— Diagram to Represent Normal Breathing-Rhythm. 

the Cheyne-Stokes type of breathing would appear as in Fig 23. 
The period of apncea may last from one to ten seconds ; then short, 
shallow respirations begin and increase rapidly, both in volume and 
in rate, until a maximum of marked dyspnoea is reached, when a 
diminution in the rate and depth of the act begins, and the patient 
gradually returns to the apnoeic state The length of the whole 
paroxysm may be from 30 to 70 seconds During the apnoeic 
period the patient is apt to drop asleep for a few seconds and the 
pupils may become contracted When the paroxysm of dyspnoea 



22 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

is at its height, he is apt to cough and shift his position restlessly, 
or in case the whole phenomenon occurs during sleep he moves un- 
easily in his sleep at this period. Modified types of the phenome- 
non also occur, in which there is a rhythmic increase and decrease 
in the depth and rapidity of respiration but without any interven- 
ing period of apnoea. This type of breathing is most often seen in 
severe cases of cardiac, renal, or cerebral disease. It is generally 
more marked at night and may occur only at that time. In chil- 
dren it appears sometimes to be physiological during sleep. As a 




Fig. 23.— Cheyne-Stokes Respiration. 

rule, it is a sign of grave prognostic significance, but patients have 
been known to recover completely after weeks or even months of 
Cheyne-Stokes breathing. 

(c) Restrained or " Catchy " Breathing. 

When the patient has a "stitch in the side," due to dry pleu- 
risy, intercostal neuralgia, or to other causes, the inspiration may 
be suddenly interrupted in the middle, owing to a seizure of pain 
which makes the patient stop breathing as quickly as he can. The 
same conditions may produce very shallow breathing as the patient 
tries to avoid the pain which a full inspiration will cause. This 
type of restrained breathing is often seen in pleurisy and pneumo- 
nia, and in the latter disease expiration is often accompanied by 
a little moan or grunt of discomfort. 

(d) Shallow and irregular breathing is often seen in states of pro- 
found unconsciousness from any cause, such as apoplexy or poison- 
ing. A few deep respirations may be followed by a number of 
shallow and irregular ones. When death is imminent in any dis- 
ease, the respiration may become very irregular and gasping, and 
it is apt to be accompanied by a peculiar nodding movement of the 



INSPECTION. 23 

head, the chin being thrown quickly upward during inspiration, and 
falling slowly during expiration. I have known bnt one patient to 
recover after this type of breathing had set in. 

After severe hemorrhage the breathing may be of a sighing type 
as well as very shallow. 

(e) Stridulous Breathing. 

A high-pitched, crowing or barking sound is heard during inspi- 
ration when there is obstruction of the entrance of air at or near 
the glottis. This type of breathing occurs in spasm or oedema of 
the glottis, " croup," laryngismus stridulus, and forms the " whoop " 
in the paroxysms of whooping-cough. Laryngeal or tracheal ob- 
structions due to foreign bodies, or tumors within or pressure from 
without the air-tubes, may cause a similar type of respiration. It 
is in these cases especially that we see the sucking-in of the inter- 
spaces mentioned above (see p. 20). 

YI. Diaphragmatic Movements. 

Litters Phenomenon. 

The normal movements of the diaphragm may be rendered vis- 
ible by the following procedure, suggested by Litten in 1892 : The 
patient lies upon his back with the chest bared and the feet pointed 
directly toward a window. Cross lights must be altogether ex- 
cluded by darkening any other windows which the room may con- 
tain 1 (see Fig. 24). The observer stands at the patient's side 
and asks him to take a full breath. As the ribs rise with the 
movement of inspiration, a short, narrow shadow moves down along 
the axilla from about the seventh to about the ninth or tenth rib. 
During the expiration the shadow rises again to the point from 
which it started, but is less easily seen. This phenomenon is to be 
seen on both sides of the chest and sometimes in the epigastrium. 

1 If it is inconvenient to move the patient's bed into the proper position 
with relation to the window, or if the foot-board interferes, or if the observa- 
tion has to be made after dark, a dark lantern or other strong light held at the 
foot of the bed answers very well. All other light must, of course, be ex- 
cluded. 



24 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

It is best seen in spare, muscular young persons of either sex, and 
is never absent in health except in those who are very fat, or who 
cannot or will not breathe deeply. The latter condition occurs in 




Fig. 24.— Litten's Diaphragm Shadow. Proper position of patient 
shadow is best seen near L. 



of observer. The 



hysteria and in some very stupid persons who cannot be made to 
understand what is meant by a full breath. In the observation of 
several thousand cases, I have never known it absent in health 
except under these conditions. 

In normal chests, the excursion of the shadow is about two and 
a half inches; with very forced breathing three and a half inches. 
The mechanism of this phenomenon is best understood by imagin- 
ing a coronal section of the thorax as seen from the front or back 
(see Fig. 25). At the end of expiration, the diaphragm lies 
flat against the thorax from its attachment up to about the sixth 
rib. During inspiration it "peels off" as it descends and allows 
the edge of the lung to come down into the chink between the dia- 
phragm and thorax. This " peeling off " of the diaphragm and the 
descent of the lung during inspiration give rise to the moving 
shadow above described. 

By thus observing the excursion of the diaphragm we can obtain 
a good deal of information of clinical value. 



INSPECTION. 



25 



In pneumonia of the lower lobe, pleuritic effusion, extensive pleu- 
ritic adhesions, or in advanced cases of emphysema, the shadow is 
absent. This is explained by the fact that in pneumonia, pleuritic 
effusion, and emphysema the diaphragm is held off from the chest 
wall so that its movements communicate no shadow. In pleuritic 
adhesions the movements of the diaphragm are prevented. In 
early phthisis I have generally' found the excursion of the dia- 
phragm diminished upon the affected side, owing to a loss of 
elasticity in the affected lung and in part probably to pleuritic 
adhesions. On the other hand, fluid or solid tumors below the dia- 
phragm, unless very large, do not prevent the descent of that muscle, 
and so do not abolish the diaphragm shadow. In cases in which 
the diagnosis is in doubt between fluid in the right pleural cavity 
and an enlargement of the liver upward or a subdiaphragmatic ab- 
seess, the preservation of the Litten's phenomenon in the latter two 
affections may be of great value in diagnosis. Very large accumu- 
lations of ascitic fluid may so far restrain the diaphragmatic move- 
ments that no shadow can be seen. Great muscular weakness or 
debility may greatly diminish, but rarely if ever prevent, the excur- 




riG. 25.— Excursion of the Diaphragm during Forced Respiration. R, Ribs ; E, position of 
the diaphragm at end of expiration ; I, position of diaphragm at end of inspiration. 



sion of the shadow. In persons who cannot be made to breathe 
deeply enough to bring it out, a hard cough will frequently render 
it visible. 

The use of this method of examination tends, to a certain ex- 
tent, to free us from the necessity of using the a-rays, inasmuch as 



26 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

it furnishes us with the means of observing the diaphragmatic 
movements, on the importance of which so much stress has been 
laid by F. H. Williams and others, much more easily and cheaply 
than with the a-rays, and upon the left side, more plainly as well. 

It also frees us to a considerable extent from the need of using 
the spirometer to determine the capacity of the lungs. 

By measuring the excursion of the phrenic shadow and taking 
account of the thoracic movement, we obtain a very fair idea of the 
respiratory capacity of the individual. 

VII. Observation of the Cardiac Movements. 
(1) The Normal Cardiac Impulse. 

With each systole of the heart there may be seen in the great 
majority of normal chests an outward movement of a small portion 
of the chest wall just inside and below the left nipple. This phe- 
nomenon is known as the cardiac impulse. 1 It is now generally 
admitted that the "apex impulse " is caused by the impact of a 
portion of the right ventricle against the chest wall and not by the 
apex of the heart itself. [The bearings of this fact, which have 
not, I think, been generally appreciated, will be discussed pres- 
ently.] The position of the maximum impulse in adults is usually 
in the fifth intercostal space just inside the nipple line. In chil- 
dren under the age of six it is often in the fourth interspace or 
behind the fifth rib; while in persons of advanced age it often de- 
scends as low as the sixth interspace. In adults it is occasionally 
absent even in perfect health and under certain pathological condi- 
tions to be later mentioned. 

(a) The position of the impulse varies to a certain extent ac- 
cording to the position of the body. If the patient lies upon the 
left side, the heart's apex swings out toward the axilla, so that 
the visible impulse shifts from one to two and one -half inches to 
the left (see Fig. 26). A slight shift to the right can also be 
brought about by lying upon the right side, and, as a rule, the im- 

1 For a more detailed description of the normal position of the cardiac 
impulse, see next page. 



INSPECTION. 



27 



pulse is less visible in the recumbent than in the upright position. 
Since the heart is lifted with each expiration by the rise of the dia- 
phragm and falls during inspiration, a corresponding change can be 
observed in the apex beat, which, in forced breathing, may shift as 
much as one interspace. Of the changes in the position of the im- 
pulse brought about by disease, I shall speak in a later paragraph. 




Fig. 26.— Showing Amount of Shifting of the Apex Impulse with Change of Position. The in- 
ner dot represents the position of the impulse when the patient lies on his back ; the outer 
dot corresponds to the position of the apex with patient on left side. 

(ft) Relation of the maximum cardiac impulse to the apex of the 
heart. — I mentioned above that the maximum cardiac impulse is not 
due to the striking of the apex of the heart against the chest wall, 
but to the impact of a portion of the right ventricle. The practical 
importance of this fact is this: When we are trying to localize the 



28 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

apex of the heart in order to determine how far the organ extends 
to the left and downward, it will not do to be gnided by the posi- 
tion of the maximum impulse, for the apex of the heart is almost 
always to be fonnd three-fourths of an inch or more farther to the 
left (see Fig. 27). This .may be proved by percussion (vide infra, 




Fig. 27,— The Inner Dot is the Maximum Cardiac Impulse. That to the right is the true apex 
of the heart, as obtained by percussion. The ribs are numbered. 



p. 58). The true position of the cardiac apex thus determined cor- 
responds usually not with the maximum impulse, but with the point 
farthest out and farthest down at which any rise and fall syn- 
chronous with the heart beat can be felt (for further discussion of 
this point see below, p. 213). 

(c) Besides the definite and localized impulse which has just 



INSPECTION. 29 

been described, it is often possible to see that a considerable section 
of the chest wall in the precordial region is lifted "en masse" 
The phenomenon is the " Herzenstoss " of the Germans, with which 
the ' ; Spitzenstoss " or apex impulse is contrasted. A variable 
amount of " Herzenstoss " can be seen and felt over any normal 
heart when it is acting rapidly and forcibly, and in thin, nervous 
subjects or in children even when the heart is beating quietly. It 
is more marked in cardiac neuroses or in cases in which the heart 
is hypertrophied and in which there is more or less stiffening of the 
ribs with loss of their natural elasticity. At times it may be 
impossible to localize any one point to which we can give the 
name of apex impulse, and what we see is the rhythmical rise and 
fall of a section of the chest as large as the palm of the hand or 
larger. 

(d) Character of the cardiac impulse. — Palpation is considerably 
more effective than inspection in giving us information as to the na- 
ture of the cardiac movements which give rise to the "apex beat," 
but even inspection sometimes suffices to show that the impulse has 
a heaving character or is of the nature of a short tap, a peristaltic 
wave, or a diffuse slap against the chest wall. In some cases a dis- 
tinct undulation can be seen passing from the apex region upward 
toward the base of the heart, or less often in the opposite direction. 

(2.) Displacement of the Cardiac Impulse. 

To one familiar with the position, extent, and character of the 
normal cardiac impulse, any displacement of this impulse from its 
normal site or any superadded pulsation in another part of the chest 
is apparent at a glance. I will consider first the commonest forms 
of dislocation of the apex impulse. 

(a) D-isplacement of the cardiac impulse due to hypertrophy and 
dilatation of the heart. — By far the most common directions of dis- 
placement are toward the left axilla, or downward. As a rule, it 
is displaced in both these directions at once. I shall return to this 
subject more in detail under the heading Cardiac Hypertrophy, but 
here I may say that enlargements of the left ventricle tend espe- 
cially to displace the apex impulse downward, while enlargements of 



30 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

the right ventricle are more commonly associated with displacement 
of the impulse toward the axilla. 

(b) Next to hypertrophy and dilatation of the heart perhaps the 
commonest cause of dislocation of the cardiac impulse is pressure 
from below the diaphragm. When the diaphragm is raised by a 
large accumulation of gas or fluid or by solid tumors of large size, 
we may see the apex beat in the fourth interspace and often an inch 
or more inside the nipple line. 

(c) Of nearly equal frequency is displacement of the heart due 
to pleuritic effusion or to pneumothorax. 

When a considerable amount of air or fluid accumulates in the 
left pleural cavity, the apex of the heart is displaced to the right 
so that it may be concealed behind the sternum or be visible beyond 
it to the right ; in extreme cases it may be dislocated as far as the 
right nipple. Eight pleuritic effusions have far less effect upon 
the position of the cardiac impulse, but when a very large amount 
of fluid accumulates we may see the impulse displaced considerably 
toward the left axilla. 

(d) I have mentioned causes tending to push the heart to the 
right, to the left, or upward. Occasionally the heart is pushed 
downward by an aneurismal tumor or a neoplasm of the mediasti- 
num. In these cases there is usually more or less displacement to 
the left as well. In old age the aorta sags or stretches a little, 
and hence the apex beat may descend to the sixth interspace. A 
similar stretching of the aorta may be produced by the weight of 
a hypertrophic d heart 

(e) Displacement of the cardiac impulse resulting from adhesions 
of the pericardium, or of the pleura, with subsequent contraction, 
occurs in fibroid phthisis and in some cases of long-standing disease 
of the pleura. Through the effect of negative pressure the heart 
may be sucked into the space formerly occupied by a portion of the 
lung, when the latter has become contracted by disease. It seems 
likely, however, that in the majority of cases adhesions between 
the pleura and pericardium play a part in such displacement. By 
these means the heart may be displaced to the right of the sternum, 
as it is by left-sided pleuritic effusion. It is often drawn upward 



INSPECTION. 31 

as well as to the right in such cases by the contraction which takes 
place in the npper part of the lung. More rarely we may see the 
heart drawn toward the left clavicle in fibroid phthisis of the left 
apex. 

(/) Distortion of the thorax due to spinal curvature or other 
causes may bring about a considerable displacement of the heart 
from its normal position. 

(g) Dextrocardia and Situs Inversus. — In rare cases a displace- 
ment of the apex impulse to the right of the sternum may be due 
either to a transposition of all viscera [the liver being found upon 
the left, the spleen upon the right, etc.], or to dextrocardia, in which 
the heart alone is transposed while the other viscera retain their 
normal places (see Fig. 138, p. 302). 

Summary. 

The apex impulse is displaced by 

(a) Hypertrophy and dilatation of the heart. 

(b) Pressure from below the diaphragm. 

(c) Air or fluid in one pleural cavity, especially the left. 

(d) Aneurism, mediastinal growths, and sagging of the aorta. 

(e) Fibroid phthisis. 
(/) Spinal curvature. 

(g) Transposition of the heart or of all the viscera. 

(3) Apex Retraction. 

Before leaving the subject of the cardiac impulse it seems best 
to speak of those cases hi which during systole we see a retraction 
of one or more interspaces at or near the point where the cardiac 
impulse normally appears. 

(ci) In by far the greater number of instances such retraction is 
due to negative pressure produced within the chest by the vigorous 
contraction of a more or less hypertrophied and dilated heart. In 
these cases the retraction is usually to be seen in several inter- 
spaces. Such retraction is not at all uncommon and usually at- 
tracts no attention. 

(b) In rarer cases several interspaces, both in the precordial 



32 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

region and in the left lower axilla and back, may be drawn in as 
a result of adhesions between the pericardium and the chest wall, 
such as form in cases of adherent pericardium and fibrous medias- 
tinitis (see below, pages 216 and 295). 

(4) Epigastric Pulsation. 

In a considerable portion of healthy adults a pulsation at the 
epigastrium synchronous with the systole of the heart is to be seen 
from time to time. Such pulsation has often been treated as evi- 
dence of hypertrophy of the right ventricle of the heart, but this I 
believe to be an error. It is not at all uncommon to find, post mor- 
tem, considerable hypertrophy of the right ventricle in cases in 
which during life no epigastric pulsation has been visible, while, on 
the other hand, the heart is frequently found normal at autopsy in 
cases in which during life there has been marked epigastric pulsa- 
tion. In some cases such pulsation is to be explained as the trans- 
mission of the heart's impulse through the liver, or as a lifting of 
that organ by the movements of the abdominal aorta. In other 
cases it is more difficult to explain. 

(5) Visible Pulsations due to Uncovering of Portions of the Heart 
Normally Covered by the Lungs. 

One of the commonest causes of visible pulsations in parts of 
the chest where normally none is to be seen is retraction of the 
lung. 

(a) It is in chlorosis, perhaps, that we most frequently see 
such pulsations. In that disease, as in other debilitated states, the 
lungs are often not adequately expanded owing to the superficiality 
of the respiration, and accordingly their margins do not cover as 
much of the surface of the heart as they do in healthy adults. 
This results in rendering visible, in the second, third, or fourth left 
interspace near the sternum, pulsations transmitted from the conus 
arteriosus or from the right ventricle. Less commonly, similar pul- 
sations may be seen on the right side of the sternum. 

(b) A rarer cause of retraction of the lungs is fibroid phthisis 
or chronic interstitial pneumonia. In these diseases a very large 



IXSPECTION. 



33 



area of pulsation may be seen in the precordial region owing to the 
entire uncovering of the heart by the retracted lung, even when the 
heart is not drawn out of its normal position. 

viii. axeurlsm and other causes of abnormal thoracic 

Pulsation. 

So far I have spoken altogether of pulsations transmitted di- 
rectly to the thorax by the heart itself, but we have also to bear in 




Fig. 28.— Position When Looking for Slight Aneurismal Pulsation. 

mind that a dilated aorta may transmit to the chest wall pulsations 
which it is exceedingly important for us to recognize and properly to 
interpret. No disease is easier to recognize than aneurism when the 
growth has perforated the chest wall and appears as a tumor exter- 
nally, but it is much more important as well as much more difficult 
to recognize the disease while it is confined within the thorax. In 
such cases, the movements transmitted from the aorta to the chest 
wall may be so slight that only the keenest and most thorough in- 
spection controlled by palpation will detect them. When slight 
pulsations are searched for, the patient should be put in a position 
3 



34 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

shown in Fig. 28, and the observer should place himself so that his 
eye is as nearly as possible on a level with the chest and looks 
across it so that he sees it in profile. In this position he can make 
out pulsations which are totally invisible if the patient sits facing 
the light. 

Pulsations due to aneurism are most apt to be seen in the first 
or second right interspace near the sternum, and not infrequently 
the clavicle and the adjacent parts may be seen to rise slightly with 
every beat of the heart, but in any part of the chest wall pulsa- 
tions due to an aneurism are occasionally to be seen, and should be 
looked for scrupulously whenever the symptoms of the case suggest 
the possibility of this disease (see below, p. 221). 

Pulsating Pleurisy. 

In cases of purulent pleurisy in which the pus has worked its 
way out betwen the ribs so that it is covered only by the skin and 
subcutaneous tissues, a pulsation transmitted from the heart may 
become visible, and the resemblance to the pulsation seen in aneu- 
rism may be confusing. Such pulsation is apt to be seen in the 
upper and front portions of the chest. Very rarely a pleuritic effu- 
sion which has not burrowed into the chest wall may transmit to 
the latter a wavy movement corresponding to the motions set up 
in the fluid by the cardiac contractions. 

IX. Inspection of the Peripheral Vessels. 

In a work dealing with diseases of the heart and lungs it is im- 
possible to avoid reference to vascular phenomena apparent in the 
neck or in the extremities, since such phenomena have a very direct 
bearing upon the interpretation of the conditions obtaining within 
the chest. Inspection plays a very large part in the study of these 
vascular phenomena. We should look for : 

(a) Venous phenomena. 

(b) Arterial phenomena. 

(c) Capillary phenomena. 



INSPECTION. 35 



(a) Inspection of the Veins. 

1. The condition of the veins of the neck is of considerable im- 
portance in the diagnosis of diseases of the heart and lungs. Where 
the tissues of the neck are more or less wasted the veins may be 
quite prominent even when no disease exists within the chest, and 
in such cases they may be more or less distended during each expi- 
ration, especially if dyspnoea or cough is present. If the veins 
are completely emptied during each expiration and on both sides of 
the neck, we can usually infer that there is an overdistention of the 
right side of the heart. When a similar phenomenon occurs on 
one side only, it may mean pressure upon one innominate vein. So 
far I have spoken of venous changes synchronous with respiration, 
but we may have also 

2. A presystolic pulsation or undulation seen either in the ex- 
ternal jugular vein or in the bulbus jugularis between the two 
attachments of the sternomastoid muscles. Such pulsation or 
undulation, which is to be seen just before each systole of the 
heart, is not necessarily anything abnormal and must be carefully 
distinguished from 

3. Systolic venous pulsation, such as occurs in one of the most 
serious valvular diseases of the heart — tricuspid regurgitation. 1 
Systolic venous pulsation is more often seen upon the right side 
than upon the left side of the neck. There may be a wave during 
the systole of the auricle and another during the systole of the ven- 
tricle, the latter closely following the former. In any case in 
which a doubt arises whether a pulsation in the veins of the neck 
is due to tricuspid regurgitation, it is well to try the experiment of 
emptying the vein by stroking it from below upward. If it imme- 
diately fills from below, we may be practically certain that tricus- 
pid regurgitation is present. In the vast majority of cases of ve- 
nous pulsation due to other causes or occurring in healthy persons 

1 A pulsating carotid may transmit an up-and-down motion to the veins 
overlying it. In such cases, if the veins be emptied by "milking" them up- 
ward, they will not refill from below. 



36 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

a vein will not refill from below if emptied in the manner above 
described. 

4. Barely, superficial veins may be seen to pulsate in other parts 
of the body, especially in aortic regurgitation, and occasionally 
large and tortuous veins may be seen pulsating upon the chest wall, 




Fig. 29.— Tortuous Veins on Chest and Abdomen. 

representing an attempt at collateral circulation when one or the 
other vena cava is compressed (Fig. 29) . 

(b) Arterial Phenomena: 

1. In thin or nervous persons pulsations are not infrequently to 
be seen in the carotids independent of any abnormal condition of 
the heart. 

2. Very violent throbbing of the carotids, more noticeable than 



INSPECTION. 



37 



that seen in health, occurs in many cases of aortic regurgitation 
and occasionally in simple hypertrophy of the heart without any 
valvular disease. From the same causes, visible pulsation may 
occur in the subclavian, axillary, brachial, and radial arteries, as 
well as in the large arterial trunks of the lower extremity. 

I lately examined a blacksmith whose heart was considerably 
enlarged by hard work, but without any valvular disease. Pulsa- 




Fig. 30.— Enlarged Tortuous Brachial Arteries (Arterio-sclerosis). 



tion was violent in all the peripheral arteries which I have just 
named. 

3. In arterio-sclerosis occurring in spare, elderly men, with or 
without aortic regurgitation, one often notices a lateral excursion of 
the tortuous brachial arteries synchronous with every heart beat. 
An up-and-down pulsation may occur at the same time. Not infre- 
quently the arteries which are stiffened by deposition of lime salts 
(see below, page 55) stand out visibly as enlarged, tortuous cords 
upon the temple and along the inner side of the biceps muscle, 
(see Figs. 30 and 31) and occasionally the course of the radial artery 



38 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

may be traced over a considerable distance in the forearm. In rare 
cases inequalities produced in the arterial wall by deposition of 
lime salts may be visible as well as palpable. 

(e) Capillar!/ Pulsation. 

If a microscopic slide is placed against the mucous membrane of 
the lower lip so as partially to blanch its surface, one may see, with 




Fig. 31. -Enlarged and Tortuous Brachial Artery ( Arterio-sclerosis) . 



each beat of the heart (in cases of aortic regurgitation and sometimes 
in other conditions), a delicate flushing of the blanched surface be- 
neath the glass slide. The same pulsation is sometimes to be ob- 
served under the finger nails, or may be still better brought out by 
drawing a pencil or other hard substance across the forehead so as 
to cause a line of hyperseniia, at the edge of which the systolic flush- 
ing occurs. This phenomenon will be referred to again when we 
come to speak of aortic regurgitation. Here it suffices to say that 
it is not in any way peculiar to that disease, and occurs occasion- 



INSPECTION. 39 

ally in health or in conditions associated with low tension in the 
peripheral arteries, as well as in any area of inflammatory hyper- 
emia (jumping toothache, throbbing felon, etc.). 

X. INSPECTION OF THE SKIN AND MUCOUS MEMBRANES. 

Light may be thrown upon the diagnosis of diseases of the chest 
by observing the color and condition of the cutaneous surfaces as 
well as of the mucous membranes. We should look for the follow- 
ing conditions : 

(1) Cyanosis. 

(2) (Edema. 

(3) Pallor. 

(4) Jaundice. 

(o) Scars and eruptions. 

(1) Cyanosis. 

By cyanosis we mean a purplish or grayish-blue tint notice- 
able especially in the face, in the lips, and under the nails. There 
are many degrees of cyanosis, from the slight purplish tinge of the 
lips, which a little overexertion or slight exposure to cold may bring 
out, up to the gray -blue color seen in advanced cases of pulmonary or 
cardiac disease, or the dark reddish-blue seen in congenital malfor- 
mations of the heart. Cyanosis makes a very different impression 
upon us when it is combined with pallor on the one hand or with 
jaundice on the other. When combined with pallor, one gets vari- 
ous ashy-gray tints, while the admixture of cyanosis and jaundice 
results in a color very difficult to describe, sometimes approaching 
a greenish hue. The commonest causes of cyanosis are : 

(a) Valvular or parietal disease of the heart. 

(b) Emphysema. 

(c) Asthma. 

(d) Pneumonia. 

(e) Phthisis. 

(/) In some persons a certain degree of cyanosis of the lips 
exists despite perfect health. This is especially true of weather- 
beaten faces and those of the so-called "full-blooded " type. 



40 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

A rare but very striking type of cyanosis is that seen in cases 
of congenital heart disease, in which the lips may be indigo blue 
in color or almost black while yet no dyspnoea is present. 

(2) (Edema. 

(Edema, or the accumulation of serous fluid in the subcutaneous 
spaces, is usually appreciated by palpation rather than by inspec- 
tion, but sometimes makes the face look very puffy, especially 
under the eyes This is not a common occurrence in diseases of 
the chest, in connection with which such oedema as takes place is 
usually to be found in the lower extremities and is appreciable 
rather by palpation i;han by inspection. If we are not familiar with 
a patient's face, we often do not perceive in it the changes of out- 
line due to oedema which, a friend would notice at once. Clothing 
is apt to leave grooves and marks wherever it presses tightly upon 
the oedematous tissues, as around the waist or over the shoulders. 
In the legs, the presence of oedema may be suggested by an unnatu- 
rally smooth, glossy appearance of the skin Such impressions, 
however, may be false unless controlled by palpation, for simple 
obesity may produce very similar appearances. 

(3) Pallor. 

Pallor suggests, though it does not in any way prove, anaemia, 
and anaemia is a characteristic of the commonest of all diseases of 
the chest — phthisis. It is also seen in certain varieties of cardiac 
disease. Pallor of the mucous membranes, as seen in the lips and 
conjunctivae, is much more apt to be a sign of real anaemia than is 
pallor of the skin. At best, pallor is only a sign which suggests to 
us to look further into the case in one or another direction, and of 
itself proves nothing of importance. 

(4) Jaundice. 

The yellowish tint which appears in the skin, and especially in 
the conjunctivae, when the escape of bile from the liver is hindered, 
is sometimes to be seen in connection with uncompensated heart 






INSPECTION. 41 

disease when the liver is greatly distended by passive congestion 
Pneumonia is occasionally complicated by jaundice; but beyond 
this I know of no special connection between this symptom and 
diseases of the chest. 

(5) Scars and Eruptions. 

In cases of suspected syphilis of the lung or bronchi the pres- 
ence of scars and eruptions suggestive of syphilis may be useful in 
diagnosis. 

XI. Enlarged Glands. 

Koutine inspection of the chest may reveal the presence of en- 
larged glands in the neck or axillae, and may thereby give us a clew 
to the nature of some intrathoracic disease ; for example, the pres- 
ence of enlarged glands in the neck, especially if there are any 
scars, sinuses, or other evidence that suppuration is going on or 
has formerly taken place in them, suggests the possibility of pul- 
monary tuberculosis or of an enlargement of the bronchial and me- 
diastinal glands. Again, malignant disease of the chest is some- 
times associated with the metastatic nodules over the clavicle, and 
a microscopic examination of them may thus reveal the nature of 
the intrathoracic disease to which they are secondary. Very large 
and matted masses of glands above the clavicle, which have never 
suppurated and have been painless and slow in their growth, sug- 
gest the presence of similar deposits in the mediastinum as a part 
of the symptom complex known as "Hodgkin's disease." The 
presence of a goitre or enlargement of the thyroid gland may ac- 
count for a well-marked dyspnoea. 

Syphilis produces general glandular enlargement ; the posterior 
cervical and the epitrochlear glands are often involved, but this is 
also the case in many diseases other than syphilis. 



CHAPTER IT. 

PALPATION AND THE STUDY OF THE PULSE. 

I Palpatio^. 

The most important points to be determined by palpation — that 
is, by laying the hand upon the surface of the chest — are : 

(1) The position and character of the apex beat of the heart. 

(2) The presence of a "thrill" (see below). 

(3) The vibrations of the spoken voice (" tactile fremitus"). 

(4) The presence of pleuritic or pericardial friction. 

Other less important data furnished by palpation will be men- 
tioned later. 

(1) The Apex Beat. 

(a) In feeling for the apex impulse of the heart, one should 
first lay the palm of the hand lightly upon the chest just below the 
left nipple. In this way we can appreciate a good deal about the 
movements of the heart, and confirm or modify what we have 
learned by inspection. One learns, in the first place, whether the 
heart beat is regular or not, and in case it is irregular, whether the 
beats are unequal in force or whether some are skipped; further, 
one gets a more accurate idea than can be obtained through inspec- 
tion regarding the character of the cardiac movements. The power- 
ful heaving impulse suggesting a hypertrophied heart, the diffuse 
slap often felt in dilatation of the right ventricle, the sudden tap 
characteristic of mitral stenosis, the deliberate thrust occasionally 
met with in aortic stenosis, may be thus appreciated. 

(b) After this, it is best to lay the tips of two or three fingers 
over the point where the maximum impulse is to be seen, and fol- 
low it outward and downward until one arrives at the point farthest 
to the left and farthest down at which it is still possible to feel 



PALPATION AND THE STUDY OF THE PULSE. 43 

any up -and- down movement. This point usually corresponds with 
the apex of the heart, as determined by percussion. It does not 
correspond with the maximum cardiac impulse, but is often to be 
found at least an inch farther to the left and downward (see above, 
Fig. 27). 

Sometimes one can localize by palpation a cardiac impulse 
which is not visible ; on the other hand, in some cases we can see 
pulsations that we cannot feel. Both methods must be used in 
every case. 

The results obtained by palpation and inspection of the apex 
region give us the most reliable data that we have regarding the 
size of the heart. Percussion may be interfered with by the pres- 
ence of gas in the stomach, of fluid or adhesions in the pleural cav- 
ity, or by the ineptness of the observer, but it is almost always pos- 
sible with a little care to make out by a combination of palpation 
and inspection the position of the apex of the heart. When we 
can neither feel it nor see it, we may have to fall back upon auscul- 
tation, considering the apex of the heart to be at or near the point 
at which the heart sounds are heard loudest. When endeavoring 
to find the apex of the heart, we must not forget that the position 
of the patient influences considerably the relation of the heart to 
the chest walls If the patient is leaning toward the left or lying 
on the left side, the apex will swing out several centimetres toward 
the left axilla. 

(2) "Thrills." 

When feeling for the cardiac impulse with the palm of the 
hand, we are in a good position to notice the presence or absence 
of a very important physical sign to which we give the name of 
"thrill." The feeling imparted to the fingers by the throat of 
a purring cat is very much like the palpable " thrill " over the pre- 
cordia in certain diseases of the heart to be mentioned later. It is 
a vibration of the chest wall, usually confined to a small area in the 
region of the apex impulse, but sometimes felt in the second right 
intercostal space or elsewhere in the precordial region. This vibra- 
tion or thrill almost always occurs intermittently, i.e., only during 



44 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

a portion of the cardiac cycle. When felt in the apex region, it 
usually occurs just before the cardiac impulse ; this fact we express 
by calling it a "presystolic thrill"; but occasionally we may feel a 
systolic thrill at the apex — one, that is, which accompanies the car- 
diac impulse. The word thrill should be used to denote only a 
purring, vibrating sensation communicated to the fingers by the 
chest wall. It is incorrect to speak of a thrill as if it were some- 
thing audible. 

We must also distinguish a purring thrill from the slight shud- 
der or jarring which often accompanies the cardiac impulse in func- 
tional neuroses of the heart or in conditions of mental excitement. 

As a rule we can appreciate a thrill more easily if we lay the 
fingers very lightly upon the chest, using as little pressure as pos- 
sible. Firm pressure may prevent the occurrence of the vibrations 
which we desire to investigate. Of the thrills felt over the base of 
the heart, more will be said in Chapter VII. 

(3) Vibrations Communicated to the Chest Wall by the Voice, 

" Tactile fremitus" is the name given to the sense of vibration 
communicated to the hand if the latter is laid upon the chest while 
the patient repeats some short phrase of words. The classical 
method of testing tactile fremitus is to ask the patient to count 
"one, two, three," or to repeat the words "ninety-nine " while the 
palm of the hand is laid flat upon the chest. The amount of fre- 
mitus to be obtained over a given part of the thorax varies, of course, 
according to the loudness of the words- spoken, and is influenced 
also by the vowels contained in them. A certain uniformity is ob- 
tained by getting the patient to repeat always the same formula. 
Thus, he is likely to use the same amount of force each time he re- 
peats them and to use approximately the same pitch of voice. 

Other things being equal, the fremitus is greater in men than 
in women, in adults than in children, and is more marked in those 
whose voices are low pitched than in those whose voices are rela- 
tively shrill The amount of fremitus also varies widely in differ- 
ent parts of the healthy chest A glance at Fig 32 will help us to 
realize this The parts shaded darkest communicate to the fingers 



PALPATIOX AND THE STUDY OF THE PULSE. 45 

the most marked fremitus, while in the parts not shaded at all, lit- 
tle or no fremitus is felt Intermediate degrees of vibration are 
represented by intermediate tints of shading. From this diagram 
we see at onee (a) that the maximum of fremitus is to be obtained 
over the apex of the right lung in front, {b) that it is greater in the 
upper part of the chest than in the lower, and somewhat greater 
throughout the right chest than in corresponding parts of the left, 




Fig. 32.— Distribution of Tactile Fremitus. 

This natural inequality of the two sides of the chest caMnot be too 
strongly emphasized. 

Comparatively little fremitus is to be felt over the scapulae be- 
hind, and still less in the precordial region in front. The outlines 
of the lungs can be quite accurately mapped out by means of the 
tactile fremitus in adults of low-pitched voice. In children, as has 
been already mentioned, fremitus is usually very slight and may be 
entirely absent, and in many women it is too slight to be of any 
considerable diagnostic value. Again, some very fat persons and 
those with thick chest walls transmit but little vibration to their 
chest walls when they speak. On the other hand, in emaciated 
patients or in those with thin-walled, flexible chests, the amount 
of fremitus is relatively great. 



46 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



Bearing in mind all these disparities — disparities both between 
persons of different age and different sex, and between the two 

sides of the chest in any one 
person — we are in a position to 
appreciate the modifications to 
which disease gives rise and 
which may be of great impor- 
tance in diagnosis. These vari- 
ations are : 

(a) Diminution or absence 
of fremitus. 

(b) Increase or absence of 
fremitus. 

(a) If the lung is pushed 
away from the chest wall by the 
presence of air or fluid in the 
pleural cavity, we get a diminu- 
tion or absence of tactile fremi- 
tus — diminution where the layer 
of fluid or air is very thin, ab- 
sence where it is of considerable 
thickness. 

(b) Solidification of the lung 
due to phthisis or pneumonia is 
the commonest cause of an in- 
crease in tactile fremitus. Fur- 
ther details as to the variations 

in amount of fremitus in different diseases may be found in later 
chapters of this book. 

(4) Friction, Pleural or Pericardial. 

In many cases of inflammatory roughening of the pleural sur- 
faces ("dry pleurisy") a grating or rubbing of the two surfaces 
upon each other may be felt as well as heard during the movements 
of respiration, and especially at the end of inspiration. Such fric- 
tion is most often felt at the bottom of the axilla, on one side or 




Fig. 33.— Showing Point (F) at Which Pleural 
Friction is Most Often Heard. 



PALPATION AND THE STUDY OF THE PULSE. 



47 



the other, where the diaphragmatic pleura is in close apposition 
with the costal layer (see Fig. 33, p. 46). 

Similarly, in roughening of the pericardial surfaces ("dry" or 
''plastic" pericarditis) it is occasionally possible to feel a grating 
or rubbing in the precordial region more or less synchronous with 
the heart's movements. Such friction is most often to be felt in 
the region of the fourth left costal cartilage (see Fig. 34). 

Palpable friction is of great value in diagnosis because it is a 
sign about which we can feel no doubt ; as such it frequently con- 




Fig. 34.— Showing Point (P) at Which Pericardial Friction is Most Often Heard. 



firms our judgment in cases in which the auscultatory signs are less 
clear. Friction sounds heard with the stethoscope may be closely 
simulated by the rubbing of the stethoscope upon the skin, but pal- 
pable friction is simulated by nothing else, unless occasionally by 

(5) Palpable Hales. 

Occasionally coarse, dry rales communicate a sensation to the 
hand placed upon the chest in the region beneath which the rales 
are produced ; to the practised hand this sensation is quite differ- 
ent from that produced by pleural friction, although the difference 
is hard to describe. 



48 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(6) Tender points upon the thorax. 

In intercostal neuralgia, dry pleurisy, necrosis of a rib, and 
sometimes in phthisis, one finds areas of marked tenderness in 
different parts of the chest. The position of the tender points in 
intercostal neuralgia generally corresponds with the point of exit 
of the intercostal nerves. These points are shown in Fig. 35. 

The tenderness in phthisis is most apt to be in the upper and 
front portions of the chest. In neurotic individuals we sometimes 
find a very superficial tenderness over parts of the thorax ; hi such 




Fig. 35.— ShowiDg Points of Exit of the Intercostal Nerves. 



cases pain is produced by very light pressure, but not by firm press- 
ure at the same point. 

(7) The presence of pulsations in parts of the chest where nor- 
mally there should be none is suggested by inspection and con- 
firmed by palpation. It is not necessary to repeat what was said 
above as to the commonest causes of such abnormal pulsations. 
When searching for slight, deep-seated pulsation (e.g., from an 
aortic aneurism), it is well to use bimanual palpation, keeping one 
hand on the front of the chest and the other over a corresponding 
area in the back. 

(8) Fluctuation or elasticity in any tumor or projection from 



PALPATION AXD THE STUDY OF THE PULSE. 49 

the chest is a very important piece of information which palpation 
may give us. 

(9) The temperature and quality of the skin are often brought 
to our attention during palpation. After a little practice one can 
usually judge the temperature within a degree or two simply from 
the feeling of the skin. Any roughness or dryness of the skin 
(myxcedema, diabetes) is easily appreciated as we pass the hand over 
the surface of the thorax or down the arms. The same manipula- 
tion often brings to our attention in cases of alcoholism an unusu- 
ally smooth and satiny quality of the cutaneous surface. 

II. The Pulse. 

Fifty years ago the study of the pulse furnished the physician 
with most of the available evidence regarding the condition of the 
heart. At present this is not the case. With the increase of our 
knowledge of the direct physical examination of the heart, the 
amount of information furnished exclusively by the pulse has pro- 
portionately decreased, until to-day, I think, it is a fact that there 
is but little to be learned by studying the pulse which could not be 
as well or better ascertained by examining the heart itself. 

Nevertheless, the radial pulse is still an important factor in 
diagnosis, prognosis, and treatment, and will remain so, because it 
gives us quickly, succinctly, and in almost every case a great deal 
of valuable information which it would take more time and trouble 
to obtain by examining the heart itself. As we feel the pulse, we 
get at once a fact of central importance in the case ; by the pulse 
the steps of our subsequent examination are guided. In emergen- 
cies or accidents the pulse gives us our bearings and tells us whether 
or not the patient's condition is one demanding immediate succor — 
e.g., hypodermic stimulation — and whether the outlook is bright or 
dark. To gather this same information by examining the heart 
itself would involve losing valuable time. 

Again, when one has to see a large number of patients in a 
short time, as in visiting a hospital ward or on the crowded days 
of private practice, the pulse is an invaluable short cut to some of 
the most important data. 
4 



50 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Moreover, there are some important inferences which the pulse 
and only the pulse enables us to make. They are not numerous, but 
their value may be great. Delay in one radial pulse when taken in 
connection with other signs may furnish decisive evidence of aneu- 
rism of the aortic arch ; aortic stenosis is a lesion which cannot be 
diagnosed unless the pulse shows certain characteristic features; 
arterial degeneration may betray its presence chiefly in the periph- 
eral arteries. 

Since, then, the condition of the pulse furnishes information of 
crucial importance in a few diseases, and is a quick, reliable, and 
convenient indication of the general condition of the circulation in 
all cases, it is essential that we should study it most carefully both 
in health and in disease. 

How to Feel the Pulse. 

(a) We usually feel for the pulse in the radial artery because 
this is the most superficial vessel which is readily available. Oc- 
casionally, as when the wrists are swathed in surgical dressings or 
tied up in a straight- jacket, we make use of the temporal, facial, 
or carotid arteries. 

(b) Both radials should always be felt at the same time. By 
making this a routine practice many mistakes are avoided and any 
difference in the two pulses is appreciated. 

(c) The tips of three fingers (never the thumb) should be laid 
upon the artery, and the following points noted : 

1. The rate of the pulse. 

2. The rhythm of the pulse (regular or irregular). 

3. The amount of force necessary to obliterate it {compressi- 
bility) . 

4. The size and shape of the pulse wave. 

5. The extent to which the artery collapses between beats 
(tension). 

6. The size and position of the artery. 

7. The condition of the artery walls. 

Each of these points will now be considered in detail. 



PALPATION AND THE STUDY OF THE PULSE. 51 

1. The Rate of the Pulse. 

In the adult male the pulse averages 72 to the minute, in the 
female 80. In children it is considerably more frequent. At birth 
it averages about 130, and until the third year it is usually above 
100. In some families as low pulse, 60 or less, is hereditary ; on the 
other hand, it is not very rare to observe a permanent pulse rate of 
110 or more in a normal adult (see below, p. 202). Exercise or emo- 
tion quickens the pulse very markedly, and after food it is somewhat 
accelerated. Some account of the causes of pathological quicken- 
ing or slowing of the pulse will be found on pages 202 and 203. 

2. Rhythm. 

The pulse may be irregular in force, in rhythm, or (as most 
commonly happens) in both respects. As a rule, irregularities in 
force are the more serious. Intermittence or irregularity in rhythm 
alone, means that the heart skips one or more beats at regular or 
irregular intervals. This may be a mere idiosyncrasy not associ- 
ated with any evidence of disease. I have known several instances 
in which a perfectly sound person has been aware of such an irregu- 
larity throughout life — the heart dropping regularly every third or 
fourth beat. Such rhythmical intermittence in health is not un- 
common. 

When beats are dropped, not at fixed intervals, but irregularly, 
the pulse waves usually vary in force as well. This combination 
of irregular cardiac rhythm with variations in the strength of the 
individual beats is very rarely seen in health and usually points to 
functional or structural disease of the heart. 

Special types of irregularity will be discussed later. 

In general it may be said (a) that irregularity in the force of 
the pulse beats is a serious sign, if overexertion and temporary 
toxic influences (tobacco, tea, etc.) can be ruled out; (b) that it is 
far more serious when occurring in connection with diseases of the 
aortic valve than in mitral disease; and (c) that it often occurs in 
connection with sclerosis of the coronary arteries and myocarditis. 



52 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

3. Compressibility . 

There is no single datum concerning the pulse more important 
than the amount of force needed to obliterate its beat. We have 
no more accurate method of measuring the compressibility of the 
pulse than the following : Let the tips of three fingers rest as usual 
on the radial artery Then gradually increase the pressure made 
upon the vessel with the finger nearest the patient's heart until the 
pulse wave is arrested and cannot be felt by the other fingers which 
rest loosely on the artery. The degree of force necessary to arrest 
the wave varies a great deal in different cases and at different times 
of day, but by trying the above manoeuvre day after day in as many 
cases as possible one comes to possess a fairly accurate mental 
standard or picture of the compressibility of the average pulse, and 
is then able to estimate in any given case whether it is more or 
less compressible than usual. 

The compressibility of the pulse is a rough measure of the mus- 
cular power of the heart's beat, and therefore gives us direct infor- 
mation about this important element in the patient's condition. 

4- The Size and Shape of the Pulse Wave. 

Of the use of the sphygmograph for representing pulse waves I 
shall speak later. The points discussed in this section are appre- 
ciable to the fingers, 

I. The size of the pulse wave — the- height to which it lifts the 
finger — depends on two factors : 

(a) The force of the cardiac contractions. 

(b) The tightness or looseness of the artery {tension). 

If the arteries are contracted and small, the pulse wave corre- 
sponds, while if they are large and relaxed, it needs only a moder- 
ate degree of power in the heart to produce a high pulse wave. If 
the tension remains constant the size of the pulse wave depends on 
the force of the heart's contraction. If the heart power remains 
constant, the size of the pulse wave depends on the degree of vas- 
cular tension. Vascular tension is estimated in ways to be de- 
scribed presently, and after allowing for it, we are enabled to esti- 



PALPATION AND THE STUDY OF THE PULSE. 53 

mate the power of the heart's contractions from the height of the 
pulse wave. 

II. The shape of the pulse wave is also of importance. 

(a) It may have a very sharp summit, rising and falling back 
again suddenly; this is known as an ill-sustained pulse, and may 
be due to a lack of sustained propulsive power in the contracting 
heart muscle, to low vascular tension, or to a combination of the 
two causes. A weak heart when stimulated by alcohol often pro- 
duces such a pulse wave — deceptively high and giving at first an 
impression of power in the heart wall, but ill sustained and easily 
compressible. An exaggeration of this type of pulse is to be felt 
in aortic regurgitation (see Fig. 102). 

(b) In sharp contrast with the above is the pulse wave which 
lifts the finger gradually and slowly, sustains it for a relatively 
long period, and then sinks gradually down again. Such a pulse 
with a " long plateau " instead of a sharp peak is to be felt most 
distinctly in aortic stenosis, less often in mitral stenosis and other 
conditions (see Fig. 107). 

(c) The dicrotic pulse wave is one in which the secondary wave, 
which the sphygmograph shows to be present in the normal pulse, 
is much exaggerated, so that a distinct " echo " of the primary 
wave is felt after each beat. If the heart is acting rapidly, this 
dicrotic wave does not have time to fall before it is interrupted by 
the primary wave of the next beat, and so appears in the sphygmo- 
graphic tracing as a part of the up-stroke of the primary wave. 
This is known as the "anacrotic pulse." 

(d) The shape of the high-tension pulse wave will be described 
hi the next paragraph. 

5. Tension. 

The degree of contraction of the vascular muscles determines 
the size of the artery and (to a great extent) the tension of the 
blood within it. But if the heart is acting feebly, there may be so 
little blood in the arteries that even when tightly contracted they 
do not subject the blood within them to any considerable degree of 
tension. To produce high tension, then, we need two factors : a 



54 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

certain degree of power in the heart muscle, and contracted arteries. 
To produce low tension we need only relaxation of the arteries, and 
the heart may be either strong or weak. 

The pulse of low tension collapses between beats, so that the ar- 
tery is less palpable than usual or cannot be felt at all. Normally, 




Fig. 36.— Sphygmographic Tracing of Low Tension Pulse. 

the artery can just be made out between beats, and any consider- 
able lowering of arterial tension makes it altogether impalpable 
except during the period of the primary wave and of the dicrotic 
wave, which is often very well marked in pulses of low tension. 
The shape of the wave under these conditions has already been 
described (see Fig. 36). 

The pulse of high tension is perceptible between beats as a dis- 
tinct cord which can he rolled between the fingers, like one of the ten- 




Fig. 37.— Sphygmographic Tracing of High Tension Pulse. 

dons of the wrist. It is also difficult to compress in most cases, but 
this may depend rather on the heart's power than on the degree 
of vascular tension. The pulse wave is usually of moderate height 
or low, and falls away slowly with little or no dicrotic wave (see 
Fig. 37). 



PALPATION A?W THE STUDY OF THE PULSE. 55 



6. The Size and Position of the Artery. 

I have often known errors to occur because a small artery is 
mistaken for a small pulse wave. The size of the branches of the 
arterial tree varies a great deal in different individuals of the same 
weight and height, and if the radial is unusually small and a hur- 
ried observation gives us the impression (true, so far as it goes) that 
there is very little in the way of a pulse to be felt, we are apt to 
conclude (wrongly, perhaps) that the heart's work is not being 
properly performed. The effort to obliterate such a pulse, how- 
ever, may set us right by showing that despite the small size of the 
vessel (and consequently of the pulse wave) it takes as much force 
as it normally does to obliterate it. Thus, a small pulse wave (in a 
congenital^ small artery) may be distinguished from a weak pulse. 
From the contracted artery of high vascular tension we distinguish 
the concjenitally small artery because the latter is not to be rolled 
beneath the fingers, and is not more than normally palpable between 
the pulse beats. 

Not infrequently the nurse reports in alarm that the patient has 
no pulse, when in reality the pulse is excellent but the artery mis- 
placed so as to be impalpable in the ordinary situation. It may be 
simply more deeply set than normal, so that the fingers cannot get 
at it, or it may run superficially over the end of the radius toward 
the "anatomical snuff box." Other anomalies are less common. 
As a rule, the other radial artery is normally placed and can be used 
as a standard, but occasionally both radials are anomalous and we 
may be compelled to use the temporal or facial instead. 

7. The Condition of the Artery Walls. 

Arterio-sclerosis is manifested in the peripheral arteries in the 
following forms : 

(a) Simple stiffening of the arteries without calcification. 

(b) Tortuosity of the arteries 

(c) Calcification. 

Simple stiffening without calcification is due to fibrous thicken- 



56 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

ing of the intima and produces a condition of the arteries not al- 
ways to be distinguished from high tension. The artery can be 
rolled under the fingers, stands out visibly between the heart's 
beats, but is not incompressible, has a smooth surface, and is not 
always tortuous. If it is tortuous as well as stiff, Ave may con- 
clude that there is endarteritis at any rate, whether or not there is 
increased tension as well. In the vast majority of cases the two 
conditions are asssociated and do not need to be distinguished. 

The normal radial artery is straight; hence any deviation is 
evidence of changes in its walls and is easily recognized as we run 
our fingers up and down the vessel. 

Calcification of the radial produces usually a beading of its sur- 
face. As we move the fingers along the artery, quickly and with 
very slight pressure, a series of transverse ridges or beads can be 
felt. The qualities of the pulse wave within can usually be appre- 
ciated fairly well, in this type of artery, but in very advanced cases 
the calcification is diffuse and converts the radial into a rigid "pipe 
stem " — absolutely incompressible — unless we break the calcified 
coat — and easily mistaken for a tendon. In such an artery no 
pulse can be felt. 

Such are the points to be observed in feeling the pulse. To 
enumerate the characteristics of the pulse in the many diseases in 
which it affords us valuable information is beyond the scope of this 
book. The qualities to be expected in the pulse in connection with 
the different diseases of the heart are described in the sections on 
those diseases. Here it will suffice to enumerate some of the con- 
ditions in which vascular tension is usually increased or diminished. 

Low tension is produced by moderate exercise, by warmth {e.g., 
a warm bath), by food. Among pathological conditions we may 
mention especially debilitated states, mental worry, and fever. 

High tension is produced by cold {e.g., cold bathing, malarial 
chills), and by constipation (in some cases). As a rule, the tension 
of the pulse increases with age and is high after the fiftieth year. 
Hysteria and migraine are often associated with increased vascular 
tension. Most frequent among pathological conditions as causes 



PALPATION AND THE STUDY OF THE PULSE. 57 

of liigli tension are chronic nephritis and arteriosclerosis with the 
various diseases in which arterio-sclerosis is a factor (gout, alcohol- 
ism, lead poisoning, diabetes of fat old people, chronic bronchitis 
with emphysema). 

Among valvular heart lesions, aortic and mitral stenosis are espe- 
cially apt to be associated with increased vascular tension. 



CHAPTEE III. 

PERCUSSION 

I. Technique. 

There is no other method of physical examination which needs 
so much practice as percussion, and none that is so seldom thor- 
oughly learned. Many physicians never succeed in acquiring a 
facility in the use of it sufficient to make them rely upon their 
results. Undoubtedly one of the greatest difficulties arises from 
the necessity of being at once active and passive — at once the per- 
cussor and the one who listens to the percussion. Students half 
unconsciously get to treat the percussion as an end in itself, and 
hammer away industriously without realizing that two-thirds of the 
attention must be given to listening, while the percussion itself 
should become semi-automatic. 

It is undoubtedly an advantage to possess a musical ear, but this 
is by no means a necessity. Some of the most accurate percussors 
that I know possess absolutely no musical ear — no ear, that is, for 
pitch — and form their judgments in percussing upon the quality or 
intensity of the note, and upon the sense of resistance. 

In this country practically all percussion is done with the fin- 
gers ; in Germany instruments are still used to a considerable ex- 
tent (see Appendix) . 

(a) Mediate and Immediate Percussion. 

Percussion may be either " mediate " or " immediate, " the lat- 
ter term referring to blows struck directly upon the chest with the 
flat of the hand, or upon the clavicles with the tip of the second 
finger. 



PERCUSSION. 



59 



(b) Methods. 

Mediate percussion (which is used ninety-nine hundredths of 
the time) is performed as follows: 

The patient should either lie down or sit with his back against 
some support. The reason of this is that for good percussion one 




Fig. 38.— Position of the Hands When Percussing the Right Apex. 



needs to press very firmly with the middle finger of the left hand 
upon the surface of the chest, so firmly that if the patient is sitting 
upon a stool without support for his back, it will need considerable 
exertion upon his part to avoid losing his balance. 



60 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

In percussing the front of the chest it is important to have the 
patient sitting or lying in a symmetrical position — that is, without 
any twist or tilting to one side. His head should point straight 
forward and his muscles must be thoroughly relaxed. Many pa- 
tients, when stripped for examination, swell out their chests and 




Position of the Hands When Percussing the Left Apex. 



sit up with a military erectness. The muscular tension thus pro- 
duced modifies the percussion note and causes an embarrassing 
multitude of muscle sounds which greatly disturb auscultation. 

Having placed the patient in an easy and symmetrical position, 
our percussion should proceed according to the following rules : 

(1) Always press as firmly as possible upon the surface of the 



PERCUSSION. 



61 



chest with the second finger of the left hand ! on the dorsum of 
which the blow is to be struck. Raise the other fingers of the left 
hand from the chest so as not to interfere with its vibrations. 

(2) Strike a quick, perpendicular, rebounding blow with the tip 
of the second finger 2 of the right hand upon the second finger of the 
left just behind the nail, imitating as far as possible with the right 
hand the action of a piano-hammer. The quicker the percussing 




Fig. 40.— The Right Way to Percuss— i. e., From the Wrist. 

finger gets away again after striking, the clearer will be the note 
obtained. 

(3) Let all the blows struck in any one part of the chest be 
uniform in force. ♦ 



^eft-handed percussors will, of course, keep the right hand upon the 
chest and strike with the left. 

2 When percussing the right apex I prefer to strike upon the thumb (see 
Figs. 38 and 39) as it is almost impossible when standing directly in front 
of the patient to fit any of the fingers comfortably into the right supraclavicular 



62 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(4) Strike from the wrist and not from the elbow (see Figs. 40 
and 41) . The wrist mnst be held perfectly loose. 

(5) Keep the percussing finger bent at a right angle as in Fig. 
42. 

The force to be used in percussion depends upon the purpose 







t 


\ 




Bfrk, ' V ^H^te— — -^ 


fe*- ... 


\^^ 



Fig. 41.— The Wrong Way to Percuss— i. e., From the Elbow. 

for which the percussion is used — that is, upon what organ we are 
percussing — and also upon the thickness of the muscles covering 
that part of the chest. For example, it is necessary to percuss 
very strongly when examining the back of a muscular man, where 
an inch or two of muscle intervenes between the finger on which 



PERCUSSION. 



63 



we strike and the king from which we desire to elicit a sound. 
Over the front of the chest and in the axillae the muscular covering 
is much thinner, and hence a lighter blow suffices. In children or 
emaciated patients, or in any case in which the muscular develop- 
ment is slight, percussion should be as light as is sufficient to elicit a 
clear sound. Heavy percussion is sometimes necessary but always 
unsatisfactory, in that the sound which it elicits comes from a rela- 
tively large area of the chest and does not therefore give us infor- 




Fig. 43.— Proper Position of the Right Hand During Percussion. 



mation about the condition of any sharply localized area. If a car- 
penter, in tapping the wall to find the position of the studs, strikes 
too hard, he will fail to find the beam, because the blow delivered 
over the spot behind which the beam is situated is so forcible as to 
bring out the resonance of the hollow parts around. It is the same 
with medical percussion. Heavy percussion is always inaccurate. 1 
It may be necessary where the muscles are very thick, but its value 

1 See also below, page 70, the lung reflex. 



64 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

is then proportionately diminished. On the other hand, it is pos- 
sible to strike so lightly that no recognizable sound is elicited at 
all. The best percussion, therefore, is that which is just forcible 
enough to elicit a clear sound without setting a large area of chest 
wall in vibration. 

The position of the patient above described applies to percus- 
sion of the front. When we desire to percuss the back, it is hn- 



/^ 


S^~^ x 


|H^ /'f/>^— 


i>) 






-.'p. jfefa. 


7w 



Fig. 43.— Proper Position of the Patient During Percussion of the Back. 



portant to get the scapulae out of the way as far as possible, since 
we cannot get an accurate idea of sounds transmitted through them. 
To accomplish this, we put the patient in the position shown in 
Fig. 43, the arms crossed upon the chest and each hand upon the 
opposite shoulder. The patient should be made to bend forward ; 
otherwise the left hand of the percussor will be uncomfortably bent 
backward and his attention thereby distracted (see Fig. 44). 

When the axillae are to be percussed, the patient should put the 
hands upon the top of the head. 



PERCUSSION. 



65 



(b) Auscultatory Percussion. 

If while percussing one auscults at the same time, letting the 
chest piece of the stethoscope rest upon the chest, or getting the 
patient or an assistant to hold it there, the sounds produced by 
percussion are greatly intensified, and changes in their volume, 
pitch, or quality are very readily appreciated. The blows must be 




Fig. 44.— Wrong Position for Percussing the Back. The patient should be bent forward. 



very lightly struck, either upon the chest itself or upon the finger 
used as a pleximeter in the ordinary way. Some observers use a 
short stroking or scratching touch upon the chest itself without 
employing any pleximeter. 

This method is used especially in attempting to map out the 
borders of the heart and in marking the outlines of the stomach. 
In the hands of skilled observers it often yields valuable results, 
5 



66 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

but one source of error must be especially guarded against. The 
line along which we percuss, when approaching an organ whose bor- 
ders ice desire to mark out, must neither approach the chest piece of 
the stethoscope nor recede from it. In other words, the line along 
which we percuss must always describe a segment of a circle whose 
centre is the chest piece of the stethoscope (see Fig. 45). If we 
percuss, as we ordinarily do, in straight lines toward or away from 
the border of an organ, our results are wholly unreliable since 
every straight line must bring the point percussed either closer to 



Percussion arc. 



Chest-piece of 
Stethoscope. 




Fig. 45.— Auscultatory Percussion, Showing the Arc along which such Percussion should he 

made. 



the stethoscope or farther from it, and the intensity and quality 
of the sounds conducted through the instrument to our ears vary 
directly with its distance from the point percussed. 

It will be readily seen that the usefulness of auscultatory per- 
cussion is limited by this source of error, and that considerable 
practice is necessary before one can get the best results from this 
method. Nevertheless it has, I believe, a place, though not a very 
important one, among serviceable methods of physical examination. 



PERCUSSION. 



67 



(c) Palpatory P 



ercussion. 



Some German observers use a method of percussion in which 
attention is fixed directly or primarily on the amount of resistance 
offered by the tissues over which percussion is made. Even in or- 
dinary percussion the amount of resistance is always noted by 
experienced percussors, but the element in sound is usually the 
main object of attention. Palpatory percussion is rather a series 
of short pushes against various points on the chest wall, but some 



Normal dulness 
of the right apex. 



Liver dulness. 



Liver flatness. 




Deep cardiac 
dulness. 



Superficial cardiac 
dulness. 



Traube's semilu- 
nar tympanitic 
space. 



Fig. 46.— Percussion Outlines in the Normal Chest. 

sound is elicited and probably enters into the rather complex judg- 
ment which follows. 

In this country palpatory percussion is but little employed. 

II. Percussion Resonance of the Normal Chest. 

The note obtained by percussing the normal chest varies a great 
deal in different areas. In Pig. 46, the parts shaded darkest are 
those that normally give least sound when percussed in the manner 
described above, while from the lightest areas the loudest and clear- 
est sound may be elicited. 



68 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



-- Upper lobe. 



„^- Lower lobe. 



,.„- Splenic area. 



(a) The sound elicited in the latter areas is known as normal or 
"vesicular" resonance, and is due to the presence of a normal 
amount of air in the vesicles of the lung underneath. If this air- 
containing lung is replaced by a fluid or solid medium, as in pleu- 
ritic effusion or pneumonia, it is much more difficult to elicit a 
sound, and such sound as is produced is 
short, high pitched, and has a feeble carry- 
ing power when compared with the sound 
elicited from the normal lung. This 
short, feeble, high-pitched sound is 
known technically as a "dull" or 
"flat" sound, flatness designating 
the extreme of the qualities that 
characterize dulness. Over the 
parts shaded dark in Pig. 46, we 
normally get a dull or flat tone, the darkest 
portions being flat and the others dull. 
The heavy shadow on the right corresponds 
to the position occupied by the liver, or 
rather by that part of it which is in imme- 
diate contact with the chest wall. The up- 
per portion of the liver is overlapped by the 
right lung (see Fig. 46), and hence at this 
point we get a certain amount of resonance 
on percussion, although the tone is not so 
clear as that to be obtained higher up. Be- 
low the sixth rib we find true flatness near 
the sternum and for a few inches to the right 
of this point. As we go toward the axilla, 
the line of lung resonance slopes down, as is seen in Fig. 47. In 
the back resonance extends to the ninth or tenth ribs. 




Fig. 47.— Position of the Left 
Lung in the Axilla. 



Normal Dull Areas. 

(b) On the left side, the main dull area corresponds to the heart, 
which at this point approaches the chest wall, and over the por- 
tion shaded darkest is uncovered by the lung. The part here 



PERCUSSION. 69 

lightly shaded corresponds to that portion of the heart which is 
overlapped by the margin of the right and left kings. 

Over the portion of the heart not overlapped by the lnng (see 
Fig. 46, p. 67) the percussion note is nearly flat to light percus- 
sion, and very dull even Avhen strongly percussed. This little 
quadrangular area is known as the "superficial cardiac space," and 
the dulness corresponding to it is referred to as the "superficial" 
cardiac dulness, while the dulness corresponding to the outlines of 
the heart itself beneath the overlapping lung margins is called the 
" deep " cardiac dulness. 

When the heart becomes enlarged, both of these areas, the deep 
and the superficial, are enlarged, the former corresponding to the 
increased size of the heart itself, while the superficial cardiac space 
is extended because the margins of the lungs are pushed aside and 
a larger piece of the heart wall comes in contact with the chest 
wall. Accordingly, either the superficial or the deep dulness may 
be mapped out as a means of estimating the size of the heart. 
Each method has its advantages and its advocates. The superficial 
dulness is easier to map out, but varies not only with the size of the 
heart, but with the degree to which the lungs are distended with 
air, or adherent to the pericardium or chest wall. What we are 
percussing is in fact the borders of the lungs at this point. 

On the other hand, the deep cardiac dulness is much more satis- 
factory as a means of estimating the size of the heart but much 
more difficult to map out. It needs a trained ear and long practice 
to percuss out correctly the borders of the heart itself, especially 
the right and the upper borders, since here we have to percuss 
over the sternum where differences of resonance are very deceptive 
and difficult to perceive. 

It is a disputed point whether light or forcible percussion should 
be used when we attempt to map out the deep cardiac dulness. 
Heavy percussion is believed by its advocates to penetrate through 
the overlapping lung margins and bring out the note corresponding 
to the heart beneath, a note which, they say, is missed altogether 
by light percussion. On the other hand, those who employ light 
percussion contend that heavy percussion sets in vibration so large 



70 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

an area of lung superficially that fine distinctions of note are made 
impossible (see above, p. 63). 

Good observers are to be found on each side of this question, 
and I have no doubt that either method works well in skilled 
hands. Personally I have found light percussion preferable. 

Whatever method we use we must percuss successive points 
along a line running at right angles to the border of the organ 
which we wish to outline until a change of note is perceived. 
Thus, if we wish to percuss out the upper border of the liver, we 
strike successive points along a line running parallel to the ster- 
num and about an inch to the right of it. 1 When a change of note 
is perceived, the point should be marked with a skin pencil ; then 
we percuss along a line parallel to the first one, and perhaps an 
inch farther out, and again mark with a dot the point at which the 
note first changes. A, line connecting the points so marked upon 
the skin represents the border of the organ to be outlined. 

If now we look at the upper part of the chest in Fig. 46, we 
notice at once that the two sides are not shaded alike : the left apex 
is distinctly lighter colored than the right. This is a very impor- 
tant point and one not sufficiently appreciated by students. The 
apex of the normal right lung is distinctly less resonant than the 
apex of the left in a corresponding position. 

In percussing at the bottom of the left axilla, we come upon a 
small oval area of dulness corresponding to that outlined in Fig. 47. 
This is the area of splenic dulness, so called, and corresponds to 
that portion of the spleen which is in contact with the chest wall. 
This dull area is to be made out only in case the stomach and colon 
are not overdistended with air. When these organs are full of gas 
as is not infrequently the case, there is no area of splenic dulness 
and the whole region gives forth, when percussed, a note of a qual- 
ity next to be described, namely, "tympanitic." 

(c) Tympanitic resonance is that obtained over a hollow body, 
like the stomach or the colon when distended with air. It is usu- 
ally of a higher pitch than the resonance to be obtained over the 

1 Or we may reverse the procedure ; percuss first over the liver and then 
work toward the lung above until the note becomes more resonant. 



PERCUSSION. 71 

normal lung, and may be elicited by percussion lighter than that 
needed to bring out the lung resonance. It differs also from the 
vesicular or pulmonary resonance in quality, in away easy to appre- 
ciate but difficult to describe. Tympanitic resonance is usually to 
be heard when one percusses over the front of the left chest near 
the ensiform cartilage and for a few inches to the left of this point 
over an area corresponding with that of the stomach more or less 
distended with air. This tympanitic area, known as " Traube's 
semilunar space" varies a great deal in size according to the contents 
of the stomach. It is bounded on the right by the liver flatness, 
above by the pulmonary resonance, on the left by the splenic dul- 
ness, and below by the resonance of the intestine, which is also 
tympanitic, although its pitch is different owing to the different 
size and shape of the intestine. 

(The right axilla shows normal lung resonance down to the 
point at which the liver flatness begins, as shown in Fig. 4.) 

In the back, when the scapulse are drawn forward, as shown in 
Fig. 43, page 64 percussion elicits a clear vesicular resonance from top 
to bottom on each side, although the top of the right lung is always 
slightly less resonant than the top of the left, and sometimes the 
bottom of the right lung is slightly less resonant than the corre- 
sponding portion of the left, on account of the presence of the liver 
on the right. 

It should be remembered, however, that in the majority of cases 
the resonance throughout the back is distinctly less than that ob- 
tained over the front, on account of the greater thickness of the 
back muscles. Yet in children or emaciated persons, or where the 
muscular development is slight, there may be as much resonance 
behind as in front. 

Importance of Ter cussing Symmetrical Points. — Since we depend 
for our standard of resonance upon comparison with a similar spot 
on the outside of the chest, it is all-important that in making such 
comparisons we should percuss symmetrical points, and not, for 
example, compare the resonance over the third rib in the right front 
with that over the third interspace on the left, since more resonance 
can always be elicited over an interspace than over a rib. This 



72 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

comparison of symmetrical points, however, is interfered with by 
the presence of the heart on one side and the liver on the other, as 
well as by the fact that the apex of the right lung is normally less 
resonant than that of the left A resonance which would be patho- 
logically feeble if obtained over the left top may be normal over the 
right Where both sides are abnormal, as in bilateral disease of 
the lung, or where fluid accumulates in both pleural cavities, we 
have to make the best comparison we can between the sound in the 
given case and an ideal standard carried in the mind. 

It must always be remembered that the amount of resonance 
obtained at any point by percussion depends upon how hard one 
strikes, as well as upon the conditions obtaining within the chest. 
A powerful blow over a diseased lung may bring out more reso- 
nance than a lighter blow over a normal lung. To strike with per- 
fect fairness and with equal force upon each side can be learned only 
by considerable practice. Furthermore, the distance from the ear 
to each of the two points, the resonance of which we are compar- 
ing, must be the same — that is, we must stand squarely in front or 
squarely behind the patient, otherwise the note coming from the 
part farther from the ear will sound duller than that coming from 
the nearer side. 

The normal resonance of the different parts of the chest can be 
considerably modified by the position of the patient, by deep breath- 
ing, by muscular exertion, and by other less important conditions. 
If, for example, the patient lies upon the left side, the heart swings 
out toward the left axilla and its dulness is extended in the same 
direction. Deep inspiration pushes forward the margins of the 
lungs so that they encroach upon and reduce the area of the heart 
dulness and liver dulness. After muscular exertion the lungs be- 
come more than ordinarily voluminous, owing to the temporary dis- 
tention brought about by the unusual amount of work thrown upon 
them. 

The area of cardiac dulness is increased in any condition involv- 
ing insufficient lung expansion. Thus, in children, in debility, 
chlorosis, or fevers, the space occupied by the lungs is relatively 
small and the dull areas corresponding to the heart and liver are 



PERCUSSION. 73 

proportionately enlarged. In old age, on the other hand, when the 
kings have lost part of their elasticity and sag down over the heart 
and liver, the percussion dulness of these organs is reduced. 

Conditions Modifying the Percussion Note in Health. — The de- 
velopment of muscle or fat as well as the thickness of the chest 
wall will influence greatly the amount of resonance to be obtained 
by percussion. Indeed, we see now and then an individual in no 
part of whose chest can any clear percussion tone be elicited. In 
women, the amount of development of the breasts has also great 
influence upon the percussion note, In children, the note is gener- 
ally clearer, and only the lightest percussion is to be used on ac- 
count of the thinness of the chest wall. In old people whose lungs 
are almost always more or less emphysematous, a shade of tym- 
panitic quality is added to the normal vesicular resonance. The 
distention of the colon with gas may obliterate the liver dulness by 
rotating that organ so that only its edge is in contact with the chest 
wall, and if there is wind in the stomach, a variable amount of 
tympany is heard on percussing the lower left front and axilla or 
even on the left back. 

If a patient is examined while lying on the side the amount of 
resonance over the lung corresponding to the side on which he 
lies is usually less than that of the side which is uppermost, because 
there is more air in the latter. Whatever the patient's position, 
the amount of resonance is also greater at the end of inspiration 
than at the end of expiration, for the reason just given. As the 
lungs expand with full inspiration, their borders move so as to 
cover a larger portion of the organs which they normally overlap. 
Portions of the chest which at the end of expiration are dull or 
flat, owing to the close juxtaposition of the heart, liver, or spleen, 
become resonant at the end of inspiration. For example, the lower 
margin of the right lung moves down during inspiration so as to 
cover a considerably larger portion of the liver. 

Percussion as a Means of Ascertaining the Movah'dit y of the Lung 
Borders. — It is often of great importance to determine not merely 
the position of the resting lung but its power to expand freely. 
This can be ascertained by percussion in the following way : The 



74 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST, 

lower border of the lung resonance, say in the axilla, is carefully 
marked out. Then percussion is made over a point just below the 
level of the resting lung and at the same time the patient is directed 
to inspire deeply If the lung expands and its border moves down, 
the percussion note will change suddenly from dull to resonant 
during the inspiration. An excursion of two or three inches can 
often be demonstrated by this method, which is especially impor- 
tant for the anterior and posterior margins of the lung. In the 
axilla Litten's phrenic shadow will give us the same information. 

The mobility of the borders of the lung, as determined by this 
method, is of considerable clinical importance, for an absence of 
such mobility may indicate pleuritic adhesions. Its amount de- 
pends upon various conditions and varies much in different indi- 
viduals, but complete absence of mobility is always pathological, 

(d) Cracked-Pot Resonance 

When percussing the chest of a crying child, we sometimes 
notice that the sound elicited has a peculiar " chinking " quality, 
like that produced by striking one coin with another, but more 
muffled. The sound may be more closely imitated, and the mode 
of its production illustrated, by clasping the hands palm to palm 
so as to enclose an air space which communicates with the outer air 
through a chink left open, and then striking the back of the under 
hand against the knee By the blow, air is forced out through the 
chink with a sound like that of metallic coins struck together. 

In disease, the cracked-pot sound is usually produced over the 
pulmonary cavity (as in advanced phthisis) from which the air is 
suddenly and forcibly expelled by the percussion stroke. 

It is much easier to hear this peculiar sound if, while percuss- 
ing, one listens with a stethoscope at the patient's open mouth. 
The patient himself holds the chest piece of the instrument just in 
front of his open mouth, leaving the auscultatory hands free for 
percussing. 



PERCUSSION. 75 

(e) Amphoric Resonance. 

A low-pitched hollow sound approximating in quality to tym- 
panitic resonance, and sometimes obtained over pulmonary cavities 
or over pneumothorax, has received the name of amphoric reso- 
nance It may be imitated by percussing the trachea or the cheek 
distended with air 

Sum mary 

The varieties of resonance to be obtained by percussing the nor- 
mal thorax are : 

(1) Vesicular resonance, to be obtained over normal lung tissue, 

(2) Tympanitic resonance, to be obtained in Traube's semilunar 
space 

(3) Diminished resonance or dulness, such as is present over the 
scapulae, and 

(4) Absence of resonance or flatness, such as is discovered when 
we percuss over the lowest ribs in the right front, 

(5) Cracked-pot resonance, sometimes obtainable over the chest 
of a crying child. 

(6) Amphoric resonance, obtainable over the trachea. 

Any of these sounds may denote disease if obtained in portions 
of the chest where they are not normally found. Each has its 
place, and becomes pathological if found elsewhere. Tympanitic reso- 
nance is normal at the bottom of the left front and axilla, but not 
elsewhere. Dulness or flatness is normal over the areas corre- 
sponding to the heart, liver, and spleen, and over the scapulce, but 
not elsewhere unless the muscular covering of the chest is enor- 
mously thick. Vesicular resonance is normal over the areas corre- 
sponding to the lungs, but becomes evidence of disease if found 
over the cardiac or hepatic areas. 

Cracked-pot resonance may be normal if produced while per- 
cussing the chest of a child, but under all other conditions, so far 
as is known, denotes disease. 

Amphoric resonance always means disease, usually pulmonary 
cavity or pneumothorax, if found elsewhere than over the trachea. 



76 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(/) The Lung Reflex. 

It must also be remembered, when percussing, that in some cases 
every forcible percussion blow increases the resonance to be ob- 
tained by subsequent blows. Any one who has demonstrated an 
area of percussion dulness to many students in succession must 
have noticed occasionally that the more we percuss the dull area, 
the more resonant it becomes, so that to those who last listen to 
the demonstration the difference which we wish to bring out is much 
less obvious than to those who heard the earliest percussion strokes. 
Abrams has referred to this fact under the name of the " lung re- 
flex," believing, partly on the evidence of fluoroscopic examination, 
that if an irritant such as cold or mustard is applied to any part of 
the skin covering the thorax, the lung expands so that a localized 
temporary emphysema is produced in response to the irritation. 
Apparently percussion has a similar effect. 

III. Sexse of Resistance. 

While percussing the chest we must be on the lookout not only 
for changes in resonance, but for variations in the amount of resist- 
ance felt underneath the finger. Normally the elasticity of the 
chest walls over the upper fronts is considerably greater and the 
sense of resistance considerably less than that felt over the liver. 
In the axillae and over those portions of the back not covered by 
the scapulae, we feel in normal chests an elastic resistance when 
percussing which is in contrast with the dead, woodeny feeling 
which is communicated to the finger when the air-containing lung 
is replaced by fluid or solid contents (pleuritic effusion, pneu- 
monia, phthisis, etc.). In some physicians this sense of resistance 
is very highly developed and as much information is obtained 
thereby as through the sounds elicited. As a rule, however, it is 
only by long practice that the sense of resistance is cultivated to a 
point where it becomes of distinct use in diagnosis. 



CHAPTER IV. 

AUSCULTATION. 

Auscultation may be practised by placing one's ear directly 
against the patient's chest (immediate auscultation) or with the 
help of a stethoscope (mediate auscultation). 

Each method has its place. Immediate auscultation is said to 
have advantages similar to those of the low power of the micro- 
scope, in that it gives us a general idea of the condition of a rela- 
tively large area of tissue, while the stethoscope may- be used, like 
the oil immersion lens, to bring out details at one or another point. 

On the other hand, I have heard it said by E. C. Janeway and 
other accomplished diagnosticians that the unaided ear can perceive 
sounds conducted from the interior of the lung — sounds quite inau- 
dible with any stethoscope — and that in this way deepseated areas 
of solidification may be recognized. 

Immediate auscultation may be objected to 

(a) On grounds of delicacy (when examining persons of the 
opposite sex). 

(b) On grounds of cleanliness (although the chest may be cov- 
ered with a towel so as to protect the auscultator to a certain 
extent). 

(c) Because we cannot conveniently reach the supraclavicular 
or the upper axillary regions in this way. 

(d) Because it is difficult to localize the different valvular areas 
and the sites of cardiac murmurs if immediate auscultation is em- 
ployed. 

On account of the latter objection the great majority of observ- 
ers now use the stethoscope to examine the heart. For the lungs, 
both methods are employed by most experienced auscultators. 



78 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(Personally, I have neve? yet learned to hear anything with my 
unaided ear which I could not hear better with a stethoscope, and 
the Bowles stethoscope seems to me to reach as large an area and 
as deep as the unaided ear. Nevertheless the weight of competent 
opinion is against me and greater experience will doubtless show 
me my mistake.) 

While learning the use of immediate auscultation it is best to 
close with the fingers the ear which is not in contact with the chest. 
With practice one comes to disregard outer noises and does not 
need to stop the ear. 

Mediate Auscultation. 

1. Selection of a Stethoscope. 

(1) It is as rash for any one to select a stethoscope without first 
trying the fit of the ear pieces in his ears as it would be to buy a 
new hat without trying it on. What suits A. very well is quite im- 
possible for B. It is true that one can get used to almost any 
stethoscope as one can to almost any hat, but it is not necessary to 
do so. The ear pieces of the ordinary stethoscope are often too 
small and rarely too large. In case of doubt, therefore, it is better 
to err upon the side of getting a stethoscope with too large rather 
than too small ends. 

(2) The binaural stethoscope, which is now almost exclusively 
used in this country, maintains its position in the ears of the aus- 
cultator either through the pressure of a rubber strap stretched 
around the metal tubes leading to the ears, or by means of a steel 
spring connecting the tubes. Either variety is usually satisfactory, 
but I prefer a stethoscope made with a steel spring (see Fig. 48) 
because such a spring is far less likely to break or lose its elasticity 
than a rubber strap. A rubber strap can always be added if this 
is desirable. It is important to pick out an instrument possessing 
a spring not strong enough to cause pain in the external meatus of 
the ear and yet strong enough to hold the ear pieces firmly in place. 
Persons with narrow heads need a much more powerful spring or 
strap than would be convenient for persons with wide heads. 



AUSCULTATION. 



79 



(3) The rubber tubing used to join the metallic tubes to the 
chest piece of the instrument should be as flexible as possible (see 
Fig. 48). Stiff tubing (see 
Fig. 49) makes it necessary 
for the auscultator to move 
his head and body from 
place to place as the exam- 
ination of the chest pro- 
gresses, while if flexible 
tubing is used the head need 
seldom be moved and a great 
deal of time and fatigue is 
thus saved. Stiff stetho- 
scopes are especially incon- 
venient when examining the 
axilla. 

(4) Jointed stethoscopes 
Avhich fold up or take apart 
should be scrupulously 
avoided. They are a delu- 
sion and a snare, apt to 
come apart at critical mo- 
ments, and to snap and creak 
at the joints when in use, 
sometimes producing in this way sounds which 
may be easily mistaken for rales. Such an in- 
strument is no more portable nor compact than 
the ordinary form with flexible tubes. It has, 
therefore, no advantages over stethoscopes made 
in one piece and possesses disadvantages which 
are peculiarly annoying. 

(5) The Chest Piece. — The majority of the 

stethoscopes now in use have a chest piece of 

hard-rubber or wood with a diameter of about seven-eighths of an 

inch. Chest pieces of larger diameter than this are to be avoided 

as they are very difficult to maintain in close apposition with thin 




Fig. 49. — C a m m a n 
Stethoscope With Stiff 
Tubing and Rubber 
Strap. 



Fig. 48. — Stethoscope 
Fitted With Long 
Flexible Tubes, Espe- 
cially Useful When 
Examining Children. 



80 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



chests. To avoid this difficulty the chest piece is sometimes made 
of soft-rubber or its diameter still further reduced. 

(6) The Bowles Stethoscojw.—fiee Figs. 50 and 51.) Within 
the last year there has been introduced an instrument which, for 
most purposes, seems to me far superior to any other form of stetho- 
scope with which I am acquainted. Its pe- 
culiarity is the chest piece, 
which consists of a very shal- 
low steel cup (see Fig. 52) 
over the mouth of which a 
thin metal plate or a bit of 
pigskin is fastened. The 
metal or pigskin diaphragm 
serves simply to prevent the 
tissues of the chest from pro- 
jecting into the shallow cup 
of the chest piece when the 
latter is pressed against the 
chest, and does not in any 
other way contribute to the 
sounds which we hear with 
the instrument. This is 
proved by the fact that we 
can hear as well even when 
the diaphragm is cracked 
across in several directions. 

With this instrument al- 
most all sounds produced 
within the chest can be heard 
much more distinctly than in 
any other variety of stethoscope. Cardiac murmurs which are in- 
audible with any other stethoscope maybe distinctly heard with this. 
Especially is this true of low-pitched murmurs due to aortic regur- 
gitation. Yet it is useful for examination not merely of the heart, 
but of the lungs as well. For any one who has difficulty in hearing 
the ordinary cardiac or respiratory sounds, or for one who is par- 




Fig. 50.— Bowles 1 Stetho 
scope. Front view. 



Fig. 51. — Bowies' 
Stethoscope. 
Back View. 



AUSCULTATION. 



81 



tially deaf, the instrument is invaluable. Its flat chest piece makes 
it very useful in listening to the posterior portions of the lungs in 
cases of pneumonia in which the patient is too sick to be turned over 
or to sit up. Without moving the patient at all we can work the 
chest piece in under the back of the patient by pressing down the 
bed-clothes, and in this way can listen to any part of the chest 
without moving the patient. A further advantage of the instru- 
ment is that it enables us to gain an approximately accurate idea 
of the heart sounds without undressing the patient. Respiratory 




Fig. 52.— Chest Piece of Bowies' Stethoscope. On the right the shallow cup communicating 
with the ear tubes. On the left the diaphragm which covers the cup, and the ring which 
holds it in place. 



sounds cannot well be listened to through the clothes, as the rub- 
bing of the latter may simnlate rales. 

There are two purposes for which I have found the Bowles 
stethoscope inferior to the ordinary stethoscope : 

(1) For listening over the apex of the lung for fine rales, e.g., 
in incipient phthisis. 

(2) For listening for superficial sounds, such as a friction rub 
of a presystolic murmur. 1 When I desire to listen for fine rales at 

1 It has frequently been observed, when listening with the ordinary stetho- 
scope, that a presystolic murmur can be better heard if only the very lightest 
pressure is made with the stethoscope. The fact that a thrill is communicated 
to the chest wall, and that that thrill is connected with the audible murmur 
explains my calling this murmur a superficial one. 

6 



82 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



an apex, for a friction rub, or for a presystolic murmur, I separate 
the chest piece of the Bowles stethoscope from the rubber tube which 
connects it with the rest of the instrument and slip on in its place 
the hard-rubber bell of an ordinary stethoscope, thereby converting 
the instrument into one of the ordinary form. With an extra hard- 
rubber bell attached or kept 
in the pocket, the instrument 
is no more bulky than an 
ordinary stethoscope, and 
far more efficient. When 
used for listening to the res- 
piration, the Bowles instru- 
ment gives us information 
similar in some respects to 
that obtained by the use of 
the free ear — that is, we are 
through it enabled to ascer- 
tain by listening at one spot 
the condition of a much 
larger area of the chest than 
can in any other way be in- 
vestigated. 

Owing to the fact that 
both cardiac and respiratory 
sounds are magnified by the 
Bowles stethoscope, this 
instrument is especially well 
adapted for use with some 
sort of an attachment whereby several sets of ear pieces are so 
joined by tubing to one chest piece that several persons may listen 
at once. Bowles' multiple stethoscope, fitted for six and for twelve 
observers, is seen in Figs. 53 and 54, and the method of its use in 
Fig. 55. In the teaching of auscultation this instrument is of great 
value, saving as it does the time of the instructor and of the stu- 
dents and the strength of the patient. The sounds conducted 
through any one of the twelve tubes used in this instrument are 




Fig. 53. 



-Bowies' Multiple Stethoscope for Six Stu- 
dents. 



AUSCULTATION. 83 

as loud as those to be heard with a single instrument of the ordi- 
nary form, although far fainter than those to be heard with a single 
Bowles stethoscope. 

II. The Use of the Stethoscope. 

Having secured an instrument which fits the ears satisfactorily, 
the beginner may get a good deal of practice by using it upon him- 




Fig. 54— Bowies' Multiple Stethoscope for Twelve Students. 

self, especially upon his own heart. The chief point to be learned 
is to disregard various irrelevant sounds and to concentrate atten- 
tion upon those which are relevant. Almost any one hears enough 
with a stethoscope, and most beginners hear too much. No great 
keenness of hearing is required, for the sounds which we listen for 
are not, as a rule, difficult to hear if attention is concentrated upon 
them. 



84 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



A. Selective Attention and What to Disregard. 

Accordingly, the art of using a stethoscope successfully depends 
upon the acquisition of two powers — 

(a) A knowledge of what to disregard, (b) A selective atten- 




Fig. 55.— Bowies' Multiple Stethoscope in Use. Twelve students listening at once. 



tion or concentration upon those sounds which we know to be of 
importance. 

Among the sounds which we must learn to disregard are the 
following : 

(1) Noises produced in the room or its immediate neighborhood, 
but not connected with the patient himself. It is, of course, easier 



AUSCULTATION. 85 

to listen in a perfectly qniet room where there are no external 
noises which need to be excluded from attention, but as the greater 
part of the student's work must be done in more or less noisy 
places, it is for the beginner a practical necessity to learn to with- 
draw his attention from the various sounds which reach his ear 
from the street, from other parts of the building, or from the room 
in which he is working. This is at first no easy matter, but can 
be accomplished with practice. 

(2) When the power to disregard external noises has been ac- 
quired, a still further selection must be made among the sounds 
which come to the ear through the tubes of the stethoscope. Noises 
produced by friction of the chest piece of the stethoscope upon the 
skin are especially deceptive and may closely simulate a pleural or 
pericardial friction sound. It is well for the student to experiment 
upon the nature and extent of such " skin rubs " by deliberately 
moving the chest piece of the stethoscope upon the skin and listen- 
ing to the sounds so produced. Mistakes can be avoided in the 
majority of cases by holding the chest piece of the stethoscope very 
firmly against the chest. This can be easily done when the patient 
is in the recumbent position, but when the patient is sitting up it 
may be necessary to press so hard with the chest piece of the 
stethoscope as to throw the patient off his balance unless he is in 
some way supported ; accordingly, it is my practice in many cases 
to put the left arm around and behind the patient so as to form a 
support, against which he can lean when the chest piece of the 
stethoscope is pressed strongly against his chest. When listening 
to the back of the chest, the manoeuvre is reversed. If the skin 
is very dry, the ribs are very prominent, or the chest is thickly 
covered with hair, it may be impossible to prevent the occur- 
rence of adventitious sounds due to friction of the chest piece 
upon the chest, no matter how firmly the instrument is held. In 
case of doubt, and in any case in which a diagnosis of pleural or 
pericardial friction is in question, the surface of the chest, at the 
point where we desire to listen, should be moistened and any hair 
that may be present thoroughly wetted with a sponge, so that it 
will lie flat upon the chest. Otherwise the friction of the hair 



86 FHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

under the chest piece of the stethoscope may simulate crepitant 
rales as closely as " skin rubs " simulate pleural friction. 

(3) The friction of the fingers of the auscultator upon the chest 
piece or on some other part of the stethoscope frequently gives rise 
to sounds closely resembling rales of one or another description. 
The nature of these sounds can be easily learned by intentionally 
moving the fingers upon the stethoscope. They are to be avoided 
by grasping the instrument as firmly as possible, and by touching it 
with as few fingers as will suffice to hold it close against the chest. 

(4) Noises produced by a shifting of the parts of the stetho- 
scope upon each other are especially frequent in stethoscopes made 
in several pieces and jointed together. A variety of snapping and 
cracking sounds, not at all unlike certain varieties of rales, may 
thus be produced, and if we are not upon our guard, may lead to 
errors in diagnosis. Stethoscopes which have no hinges and which 
do not come apart are far less likely to trouble us in this way. 

(5) When a rubber band is used to press the ear pieces more 
firmly into the ears, a very peculiar sound may be produced by the 
breathing of the auscultator as it strikes upon the rubber strap. It 
is a loud musical note, and may be confused with coarse, dry rales. 

When one has learned to recognize and to disregard the noises 
produced in the ways above indicated, there is still one set of 
sounds which are very frequently heard, yet which have no signifi- 
cance for physical diagnosis, and must therefore be disregarded ; I 
refer to 

B. Muscle Sounds. 

Patients who hold themselves very erect while being exam- 
ined, or who for any reason contract the muscles of that portion of 
the chest over which we are listening, produce in these muscles a 
very peculiar and characteristic set of sounds. The contraction of 
any muscle in the body produces sounds similar in quality to those 
heard over the chest, but of less intensity. 

Those who have the faculty of contracting the tensor tympani 
muscle at will can at any time listen to a typical muscle sound. 



AUSCULTATION. 87 

Or close both ears with the fingers and strongly contract the rnas- 
seter muscle, with the teeth clenched. A high-pitched muscle 
sound will be heard. 

It is well also to have a patient contract one of the pectorals 
and then listen to the sound thus produced. In some cases a con- 
tinuous, low-pitched roar or drumming is all that we hear ; in other 
cases we hear nothing but the breath sounds during expiration, 
while during inspiration the breath sound is obscured by a series of 
short, dull, rumbling sounds, following each other at the rate of 
from five to ten in a second. Occasionally the sound is like the 
puffing of the engine attached to a pile-driver, or like a stream of 
water falling upon a sheet of metal just slowly enough to be sepa- 
rated into drops and heard at a considerable distance. As already 
mentioned, we are especially apt to hear these muscle sounds dur- 
ing forced inspiration, owing to the contraction of voluntary mus- 
cles during that portion of the respiratory act. They are most 
often heard over the upper portion of the chest (over the pectorals 
in front and over the trapezius behind), but in some persons no 
part of the chest is free from them. It is a curious fact that we 
are not always able to detect by sight or touch the muscular con- 
tractions which give rise to these sounds, and the patient himself 
may be wholly unaware of them. Under such circumstances they 
are not infrequently mistaken for rales, and I am inclined to think 
that many of the sounds recorded as "crumpling," "obscure," 
"muffled," "distant," or "indeterminate" rales are in reality due 
to muscular contractions. The adjectives "muffled " and " distant " 
give us an inkling as to the qualities which distinguish muscular 
sounds from rales. Bales are more clean cut, have a more distinct 
beginning and end, seem nearer to the ear, and possess more of a 
crackling or bubbling quality than muscle sounds. 

I have made no attempt exhaustively to describe all the sounds 
due to muscular contractions and conducted to the ear by the steth- 
oscope, but have intended simply to call attention to the importance 
of studying them carefully. 



88 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

C. Other Sources of Error. 

Another source of confusion, which for beginners is very trouble- 
some, especially if they are using the ordinary form of stethoscope 
with a bell-shapecl chest piece, arises in case the chest piece is not 




Fig. 56.— Showing an Accident to be Avoided. (Stethoscope disconnected.) 

held perfectly in apposition with the skin. If, for example, the 
stethoscope is slightly tilted to one side so that the bell is lifted 
from the skin at some point, or if one endeavors to listen over 
a very uneven part of the chest on which the bell of the stethoscope 
cannot be made to rest closely, a roar of external noises reaches the 
ear through the chink left between the chest piece and the chest. 



AUSCULTATION. 



89 



After a little practice one learns instantly to detect this condition 
of things and so to shift the position of the chest piece that exter- 
nal noises are totally excluded ; but by the beginner, the peculiar 
babel of external noises which is heard whenever the stethoscope 
fails to fit closely against the chest is not easily recognized, and 




Fig. 57.— Accident to be Avoided. (Stethoscope kinked.) 

hence he tends to attribute some of these external sounds to diseased 
conditions within the chest. 

Again, it is not until we have had considerable practice that our 
sense of hearing comes instantly to tell us when something is wrong 
about the stethoscope itself ; when, for example, one of the tubes 
is blocked, kinked, or disconnected (see Figs. 56 and 57), or when 
we are holding the stethoscope upside down, so that the ear pieces 
point downward instead of upward (see Figs. 58 and 59) . It is only 
when we have learned through long practice about how much we 



90 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

ought to hear at a given point in the normal chest that we recognize 
at once the fact that we are not hearing as much as ice should, in 




fig. 



Stethoscope Held Right Side Up. 



case some one of the above accidents has happened. Many begin- 
ners do not listen long enough in any one place, but move the chest 
piece of the stethoscope about rapidly from point to point, as they 
have seen experienced auscultators do; but it is remarkable how 
much more one can hear at a given point by simply persevering and 
listening to beat after beat, or breath after breath. It is sometimes 







Fig. 59.— Stethoscope Held Wrong Side Up. 



difficult to avoid the impression that the sounds themselves have 
grown louder as we continue to listen, especially if we are hi any 



AUSCULTATION. 91 

doubt as to what we hear. Therefore, if we hear indistinctly, it is 
important to keep on listening, and to fix the attention successively 
upon each of the different elements in the sounds under consideration. 
In difficult cases we should use every possible aid toward concen- 
tration of the attention, and where it is possible, all sources of dis- 
traction should be eliminated. Thus, in any case of doubt, I think 
it is important for the auscultator to get himself into as comfort- 
able a position as he can, so that his attention is not distracted by 
his own physical discomforts. Many auscultators shut their eyes 
when listening hi a difficult case so as to avoid the distraction of 
impressions coming through the sense of sight. It goes without 
saying that if quiet can be secured in the room where we are work- 
ing, and outside it as well, we shall be enabled to listen much more 
profitably. 

AUSCULTATION OF THE LUNGS. 

In the majority of cases ordinary quiet breathing is not forcible 
enough to bring out the sounds on which we depend for the diag- 
nosis of the condition of the lungs. Deep or forced breathing is 
what we need. 

As a rule, the patient must be taught how to breathe deeply, 
which is best accomplished by personally demonstrating the act of 
deep breathing and then asking him to do the same. Two difficul- 
ties are encountered : 

(a) The patient may blow out his breath forcibly and with a 
noise, since that is what he is used to doing whenever he takes a 
long breath under ordinary circumstances ; or 

(b) It may be that he cannot be made to take a deep breath at 
all. The first of these mistakes alters the sounds to be heard with 
the stethoscope in any part of the chest by disturbing both the 
rhythm and the pitch of the respiratory sounds. In this way the 
breathing may be made to sound tubular or asthmatic throughout a 
sound chest. This difficulty can sometimes be overcome by demon- 
strating to the patient that what you desire is to have him take a 
full breath and then simply let it go, but not blow it forcibly out. 
In some cases the patient cannot be taught this, and we have to get 



92 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

on the best we can despite his mistakes. When he cannot be made 
to take a fnll breath at all, we can often accomplish the desired re- 
sult by getting him to cough. The breath just before and after a 
cough is often of the type we desire. The use of voluntary cough 
in order to bring out rales will be discussed later on. Another use- 
ful manoeuvre is to make the patient count aloud as long as he can 
with a single breath. The deep inspiration which he is forced to 
take after this task is of the type which we desire. 

I. Respiratory Types. 

In the normal chest two types of breathing are to be heard : 

(1) Tracheal, bronchial, or tubular breathing. 

(2) Vesicular breathing. 

Tracheal, bronchial, or tabular breathing is to be heard in normal 
cases if the stethoscope is pressed against the trachea, and as a rule 




Fig. 60.— Situation of the Trachea and Primary Bronchi. 

it can also be heard over the situation of the primary bronchi, in 
front or behind (see Figs. 60 and 61) . 

Vesicular breathing is to be heard over the remaining portions of 
the lung — that is, in the front of the thorax except where the heart 



AUSCULTATION. 93 

and the liver come against the chest wall, in the back except where 
the presence of the scapulae obscures it, and throughout both axillae. 

(1) Characteristics of Vesicular Breathing. 

Vesicular breathing — that heard over the air vesicles or paren- 
chyma of the lung — has certain characteristics which I shall try to 
describe in terms of intensity, duration, and pitch. 




Fig. 61.— Situation of the Trachea and Primary Bronchi. 

Of the quality of the sounds heard over this portion of the lung 
there is little can be said ; it sounds something like the swish of the 
wind in a grove of trees some distance off, and hence is sometimes 
spoken of as "breezy." 

The intensity, duration, and pitch of the inspiration as compared 
with that of the expiration may be represented as in Fig. 62. In 
this figure, as in all those to be used in description of respiratory 
sounds — 

(1) I represent the inspiration by an up-stroke and the expira- 
tion by a down-stroke (see the direction of the arrows in Fig. 62). 

(2) The length of the up-stroke as compared with that of the 
down-stroke corresponds to the length of inspiration compared with 
expiration. 



94 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(3) The thickness of the up -stroke as compared with the down- 
stroke represents the intensity of the inspiration as compared with 
the expiration. 

(4) The pitch of inspiration as compared with that of expi- 
ation is represented by the sharpness of the angle which the up- 



Fig. 62.— Vesicular Breath- Fig. 63.— Distant Vesicular Fig. 64. -Exaggerated Ve- 

ing. Breathing. sicular Breathing. 

stroke makes with the perpendicular as compared with that which 
the down-stroke makes with the perpendicular. The pitch of a 
roof may be thought of in this connection to remind us of the mean- 
ing of these symbols. 

If now we look again at Fig. 62 we see that when compared 
with expiration (the down-stroke), the inspiration is — 

(a) More intense. 

(b) Longer. 

(c) Higher pitched. 

Our comparison is invariably made between inspiration and ex- 
piration, and not with any other sound as a standard. 

Now, this type of breathing (which, as I have said, is to be 
heard over every portion of the lung except those portions imme- 
diately adjacent to the primary bronchi), is not heard everywhere 
with equal intensity. It is best heard below the clavicles in front, 
in the axillae, and below the scapulae behind, but over the thin, 
lower edges of the lung, whether behind or at the sides, it is 
feebler, though still retaining its characteristic type as revealed in 
the inspiration and expiration in respect to intensity, duration, and 
pitch. To represent distant vesicular breathing graphically we 
have only to draw its symbol on a smaller scale (see Fig. 63). On 



AUSCULTATION. 



95 



the other hand, when one listens to the lungs of a person who has 
been exerting himself strongly, one hears the same type of respira- 
tion, but on a larger scale, which may then be represented as in 
Fig. 64. This last symbol may also be used to represent the respi- 
ration which we hear over normal but thin- walled chests ; for ex- 
ample, in children or in emaciated persons. It is sometimes known 
as " exaggerated " or "puerile" respiration. When one lung is 
thrown out of use by disease so that increased work is brought 
upon the other, the breath sounds heard over the latter are increased 
and seem to be produced on a larger scale. Such breathing is some- 
times spoken of as " rough " breathing. 

It is very important to distinguish at the outset between the 
different types of breathing, one of which I have just described, and 
the different degrees of loudness with which any one type of breath- 
ing may be heard. 

(2) Bronchial or Tracheal Breathing in Health. 

Bronchial breathing may be symbolically represented as in Fig. 
65, in which the increased length of the down stroke corresponds 
to the increased duration of expiration, and the greater thickness 




Fig. 65.— Bronchial Breath- 
ing of Moderate Intensity. 



Fig. 



—Distant Bronchial 
Breathing. 



Fig. 67.— Very Loud Bron- 
chial Breathing. 



of both lines corresponds to the greater intensity of both sounds, 
expiratory and inspiratory, while the sharp pitch of the " gable ".on 
both sides of the perpendicular corresponds to the high pitch of 
both sounds. Expiration, it will be noticed, slightly exceeds inspi- 
ration both in intensity and pitch, and considerably exceeds it in 
duration, while as compared with vesicular breathing almost all the 



96 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

relations are reversed. Bronchial breathing has also a peculiar 
quality which can be better appreciated than described. 

In the healthy chest this type of breathing is to be heard if one 
listens over the trachea or primary bronchi (see above, Fig. 60), 
but practically one hardly ever listens over the trachea and bronchi 
except by mistake, and the importance of familiarizing one's self 
with the type of respiration heard over these portions of the chest 
is due to the fact that in certam diseases, especially in pneumonia 
and phthisis, we may hear bronchial breathing over the parenchyma 
of the lung where normally vesicular breathing should be heard. 

The student should familiarize himself with each of these types 
of breathing, the vesicular and the bronchial, concentrating his at- 
tention as he listens first upon the inspiration and then upon the 
expiration, and comparing them with each other, first in duration, 
next in intensity, and lastly in pitch. To those who have not a 
musical ear, high-pitched sounds convey the general impression of 
being shrill, while low-pitched sounds sound hollow and empty, but 
the distinction between intensity and pitGh is one comparatively 
difficult to master. Distant bronchial breathing may be repre- 
sented in Fig. 66, and is to be heard over the back of the neck 
opposite the position of the trachea and bronchi. Fig. 61 repre- 
sents very loud bronchial breathing such as is sometimes heard in 
pneumonia. 

(3) Broncho- Vesicular Breathing in Health. 

As indicated by its name, this type of breathing is intermediate 
between the two just described, hence the terms "mixed breath- 
ing," or " atypical breathing " (" unbestimmt ") . Its characteristics 
may be symbolized as in Fig. 68. In the normal chest one can be- 
come familiar with broncho-vesicular breathing, by examining the 
apex of the right lung, or by listening over the trachea or one of the 
primary bronchi, and then moving the stethoscope half an inch at 
a time toward one of the nipples. In the course of this journey 
one passes over points at which the breathing has, in varying de- 
grees, the characteristics intermediate between the bronchial type 
from which we started and the vesicular type toward which we are 



AUSCULTATION. 



97 



moving. Expiration is a little longer, intenser, or higher pitched 
than in vesicular breathing, and inspiration a little shorter, feebler, 





A 



Fig. 68.— Two Common Types of Broncho- 
Vesicular Breathing. 



Fig. 



-Distant Broncho-Vesicular Breath- 
ing. 



or lower pitched ; but since these characteristics are variously com- 
bined, there are many subvarieties of broncho-vesicular breathing. 
Fig. 69 represents two types of distant broncho-vesicular breath- 
ing. 

(4) Emphysematous Breathing. 

A glance at Fig. 70 will call up the most important features of 
this type of respiration. The inspiration is short and somewhat 
feeble, but not otherwise remarkable. The expiration is long, 
feeble, and low pitched. This type of breathing is the rule in 
elderly persons, particularly those of the male sex. 

(5) Asthmatic Breathing. 

Fig. 71 differs from emphysematous only in the greater intensity 
of the expiration. In this type of breathing, however, both sounds 



Fig. 70.— Emphysematous Breathing. 



Fig. 



71. — Asthmatic Breathing. 8, s, 
squeaking (musical) rales. 



are usually obscured to a great extent by the presence of piping and 
squeaking rales (see below) . 
7 



98 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(6) Interrupted or " Cogwheel " Breathing. 

As a rule, only the inspiration is interrupted, being transformed 
into a series of short, jerky puffs as shown in Fig. 72. Very rarely 
the expiration is also divided into segments. When heard over the 
entire chest, cogwheel breathing is usually the result of nervous- 
ness, fatigue, or chilliness on the patient's part. With the removal 
of these causes this type of respiration then disappears. If, on the 
other hand, cogwheel respiration is confined to a relatively small 
portion of the chest, and remains present despite the exclusion of 




> 



Fig. 72.— Cogwheel Breathing. 



Fig. 73.— Metamorphosing Breathing. 



fatigue, nervousness, or cold, it points to a local catarrh in the finer 
bronchi such as to render difficult the entrance of air into the alve- 
oli. As such, it has a certain significance in the diagnosis of early 
phthisis, a significance similar to that of rales or other signs of 
localized bronchitis (see below) . 



(7) Amphoric or Cavernous Breathing (see below, p. 103). 

(8) Metamorphosing Breathing. 

Occasionally, while we are listening to an inspiration of normal 
pitch, intensity, and quality, a sudden metamorphosis occurs and the 
type of breathing changes from vesicular to bronchial or amphoric 
(see Fig. 73), or the intensity of the breath sounds may suddenly 
be increased without other change. These metamorphoses are usu- 
ally owing to the fact that a plugged bronchus is suddenly opened 
by the force of the inspired air, so that the sounds conducted 
through it become audible. 



AUSCULTATION. 99 

II. Differences between the Two Sides of the Chest. 

Over the apex of the right lung — that is, above the right clavi- 
cle in front, and above the spine of the scapula behind — one hears 
in the great majority of normal chests a distinctly broncho-vesicu- 
lar type of breathing. In a smaller number of cases this same 
type of breathing may be heard just below the right clavicle. 
These facts cannot be too strongly insisted upon, since it is only 
by bearing them in mind that we can avoid the mistake of diagnos- 
ing a beginning consolidation of the right apex where none exists. 
Breath sounds which are perfectly normal over the right apex would 
mean serious disease if heard over similar portions of the left lung. 
It will be remembered that the apex of the right lung is also duller 
on percussion than the corresponding portion of the left, and that 
the voice sounds and tactile fremitus are normally more intense on 
the right (see Fig. 32). 

Occasionally one finds at the base of the right lung posteriorly 
a slightly feebler or more broncho -vesicular type of breathing than 
in the corresponding portion of the left lung. 

III. Pathological Modifications of Vesicular Breathing. 

Having now distinguished the different types of breathing and 
described their distribution in the normal chest, we must return to 
the normal or vesicular breathing in order to enumerate certain of 
its modifications which are important in diagnosis. 

(1) Exaggerated Vesicular Breathing (" Compensatory " Breathing). 

(a) It has already been mentioned . that in children or in adults 
with very thin and flexible chests the normal breath sounds are 
heard with relatively great distinctness ; also that after any exer- 
tion which leads to abnormally deep and forcible breathing a simi- 
lar increase in the intensity of the respiratory sounds naturally 
occurs. 

(b) The term "compensatory breathing" or "vicarious" breath- 
ing, refers to vesicular breathing of an exaggerated type, such as is 
heard, for example, over the whole of one lung when the other lung 

LtTC 



100 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

is thrown out of use by the pressure of an accumulation of air or 
fluid in the pleural cavity. A similar exaggeration of the breathing 
upon the sound side takes place when the other lung is solidified, 
as by tuberculosis, pneumonia, or malignant disease, or when it is 
compressed by the adhesions following pleuritic effusion, or by 
a contraction of the bones of that side of the chest such as occurs 
in spinal curvature. 

(2) Diminished Vesicular Breathing. 

The causes of a diminution in the intensity of the breath sounds 
without any change in their type are very numerous. I shall men- 
tion them in an order corresponding as nearly as possible to the 
relative frequency of their occurrence. 

(a) Fluid, Air, or Solid in the Pleural Cavity. — Probably the 
commonest cause for a diminution or total abolition of normal 
breath sounds is an accumulation of fluid in the pleural cavity such 
as occurs in inflammation of the pleura or by transudation ( hydro - 
thorax). In such cases the layer of fluid intervening between the 
lung and the stethoscope of the auscultator causes retraction of the 
lung so that little or no vesicular murmur is produced in it, and 
hence none is transmitted to the ear of the auscultator. An ac- 
cumulation of air in the pleural cavity (pneumothorax) may dimin- 
ish or abolish the breath sounds precisely as a layer of fluid does ; 
in a somewhat different way a thickening of the costal or pulmo- 
nary pleura or a malignant growth of the chest wall may render 
the breath sounds feeble or prevent their being heard because the 
vibrations of the thoracic sounding-board are thus deadened. Which- 
ever of these causes, fluid or air or solid, intervenes between the lung 
and the ear of the auscultator, the breath sounds are deadened or 
diminished without, as a rule, any modification of their type. The 
amount of such diminution depends roughly on the thickness of the 
layer of extraneous substance, whether fluid, air, or solid. 

Total absence of breath sounds may therefore be due to any one 
of these causes, provided the layer intervening between the lung and 
chest wall is of sufficient thickness to produce complete atelectasis 
of the lung or to deaden the vibrations of the chest wall. 



AUSCULTATION. 101 

(b) Emphysema of the lung, by destroying its elasticity and re- 
ducing the extent of its movements, makes the breath sounds rela- 
tively feeble, but seldom, if ever, abolishes them altogether. 

(c) In bronchitis the breath sounds are usually considerably di- 
minished owing to the filling up of the bronchi with secretion. 
This diminution, however, usually attracts but little attention, 
owing to the fact that the bubbling and squeaking sounds, which 
result from the passage of air through the bronchial secretions, dis- 
tract our notice to such an extent that we find it difficult to con- 
centrate attention upon the breath sounds, even if we do not forget 
altogether to listen to them. When, however, we succeed in listen- 
ing through the rales to the breath sounds themselves, we usually 
notice that they are very feeble, especially over the lower two- 
thirds of the chest. (Edema of the lung may diminish the breath 
sounds in a similar way. 

(77) Pain in the thorax, such as is produced by dry pleurisy or 
intercostal neuralgia, diminishes the breath sounds because it leads 
the patient to restrain, so far as possible, the movements of his 
chest, and so of his lungs. If, for any other reason, the full ex- 
pansion of the lung does not take place, whether on account of the 
feebleness of the respiratory movements or because the lung is me- 
chanically hindered by the presence of pleuritic adhesions, the 
breath sounds are proportionately feeble. 

(e) Occlusion of the upper air passages, as by spasm or oedema 
of the glottis, renders the breathing very feeble on both sides of 
the chest. If one of the primary bronchi is occluded, as by a for- 
eign body or by pressure of a tumor or enlarged gland from without, 
we get a unilateral enfeeblement of the breathing over the corre- 
sponding lung. 

(/) Occasionally a paralysis of the muscles of respiration on one 
or both sides is found to result in a unilateral or bilateral enfeeble- 
ment of the breathing. 

It should be remembered, when estimating the intensity of the 
breathing, that the sounds heard over the right lung are, as a rule, 
slightly more feeble than those heard over the left lung in the 
normal chest. 



102 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



IV. Bronchial or Tubular Breathing in Disease. 

(a) I have already described the occurrence of bronchial breath- 
ing in parts of the normal chest, namely, over the trachea and pri- 
mary bronchi. In disease, bronchial breathing may be heard else- 
where in the chest, and usually points to solidification of that portion 
of lung from which it is conducted. It is heard most commonly in 
phthisis (see below, p. 249). 

(b) Croupous pneumonia is probably the next most frequent 
cause of bronchial breathing, although by no means every case of 
croupous pneumonia shows this sign. For a more detailed account 
of the conditions under which it does or does not occur in croupous 
pneumonia, see below, p. 239. Lobular pneumonia is rarely mani- 
fested by tubular breathing. 

(c) In about one -third of the cases of pleuritic effusion distant 
bronchial breathing is to be heard over the fluid. On account of 
the feebleness of the breath sounds in such cases they are often 
put down as absent, as we are so accustomed to associate intensity 
with the bronchial type of breathing. One should be always on 
the watch for any degree of intensity of bronchial breathing from 
the feeblest to the most distinct. 

(d) Rarer causes of bronchial breathing are hemorrhagic infarc- 
tion of the lung, syphilis, or malignant disease, any one of which 
may cause a solidification of a portion of the lung. 

V. Broncho-Yesicular Breathing in Disease. 

Respiration of this type should be carefully distinguished from 
puerile or exaggerated breathing, in which we hear the normal vesic- 
ular respiration upon a large scale. I have already mentioned 
that broncho-vesicular breathing is normally to be heard over the 
apex of the right lung. In disease, broncho-vesicular breathing is 
heard in other portions of the lung, and usually denotes a moderate 
degree of solidification of the lung, such as occurs in early phthisis 
or in the earliest and latest stages of croupous pneumonia. In cases 
of pleuritic effusion, one can usually hear broncho -vesicular breath- 



AUSCULTATION. 103 

ing over the upper portion of the affected side, owing to the retrac- 
tion of the lung at that point. 

VI. Amphoric Breathing (Amphora = A Jar). 

Eespirations having a hollow, empty sound like that produced 
by blowing across the top of a bottle, are occasionally heard in dis- 
ease over pulmonary cavities (e.g., in phthisis) or in pneumothorax, 
i.e. } under conditions in which the air passes in and out of a large 
empty cavity within the chest. Amphoric breathing never occurs 
in health. The pitch of both sounds is low, but that of expiration 
lower than that of inspiration. The intensity and duration of the 
sounds vary, and the distinguishing mark is their quality which 
resembles that of a whispered "who." 

VII. Bales. 

The term " rales " is applied to sounds produced by the passage 
of air through bronchi which contain mucus or pus, or which are 
narrowed by swelling of their walls. 1 Rales are best classified as 
follows : 

(1) Moist or bubbling rales, including (a) coarse, (b) medium, 
and (c) fine rales. 

(2) Dry or crackling rales (large, medium, or fine) . 

The smallest varieties of this type are known as " crepitant " or 
" subcrepitant n rales. 

(3) Musical rales (high or low pitched). 

Each of these varieties will now be described more in detail. 

(1) Moist or Bubbling Rales. 

The nature of these is sufficiently indicated by their name. 
The coarsest or largest bubbles are those produced in the trachea, 
and ordinarily known as the "death rattle." Tracheal rales occur 

1 Riles are of all auscultatory phenomena the easiest to appreciate, pro- 
vided we exclude various accidental sounds which may be transmitted to the 
ear as a result of friction of the stethoscope against the skin or against the 
fingers of the observer. (See above, page 80.) 




104 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

in any condition involving either profound unconsciousness or very 
great weakness, so that the secretions which accumulate in the 
trachea are not coughed out. Tracheal rales are by no means a 
sure precursor of death, although they are very common in the 
moribund state. They can usually be heard at some distance from 
the patient and without a stethoscope. In catarrh of the larger 
bronchi large bubbling rales are occasionally to be 
heard. In phthisical cavities one sometimes hears 
coarse, bubbling rales of a very metallic and gurgling 
quality (see below, p. 252). The finer grades of moist 
rales correspond to the finer bronchi. 

In the majority of cases moist rales are most numer- 

fig 74 — Expio- ous during inspiration and especially during the latter 

sion of Fine part of this act. Their relation to respiration may be 

(/inspiration, represented graphically as in Fig. 74, using large dots 

for coarse rales and small dots for fine rales. Musical 

rales can be symbolized by the letter S (squeaks). 

(2) Crackling Rales. 

These differ from the preceding variety merely by the absence 
of any distinct bubbling quality. They are usually to be heard in 
cases of bronchitis in which the secretions are unusually tenacious 
and viscid. They are especially apt to come at the end of inspira- 
tion, a large number being evolved in a very short space of time, so 
that one often speaks of an " explosion of fine crackling rales " at 
the end of inspiration. Crackling rales are to be heard in any one 
of the conditions in which bubbling rales occur, but are more fre- 
quent in tuberculosis than in simple bronchitis. 

Crepitant rales, which represent the finest sounds of this type, 
are very much like the noise which is heard when one takes a lock 
of hair between the thumb and first finger and rubs the hairs upon 
each other while holding them close to the ear. A very large num- 
ber of minute crackling sounds is heard following each other in 
rapid succession. To the inexperienced ear they may seem to blend 
into a continuous sound, but with practice the component parts may 



AUSCULTATION. 105 

be distinguished. This type of rales is especially apt to occur dur- 
ing inspiration alone, but not very infrequently they are heard 
during expiration as well. From subcrepitant rales they are dis- 
tinguished merely by their being still finer than the latter. ' Sub- 
crepitant rales are often mixed with sounds of a somewhat coarser 
type, while crepitant rales are usually all of a size. If the 
chest is covered with hair, sounds precisely like these two varieties 
of rales may be heard when the stethoscope is placed upon the hairy 
portions. To avoid mistaking these sounds for rales one must 
thoroughly wet or grease the hair. 

Crepitant Rales in Atelectasis. 

Crepitant and subcrepitant rales are very often to be heard along 
the thin margins of the lungs at the base of the axillae and in the 
back, especially when a patient who is breathing superficially first 
begins to take deep breaths. In such cases, they usually disappear 
after the few first respirations, and are then to be explained by the 
tearing apart of the slightly agglutinated surfaces of the finer bron- 
chioles. 

It is by no means invariably the case, however, that such sub- 
crepitant rales are merely transitory in their occurrence. In a large 
number of cases they persist despite deep breathing. The fre- 
quency of subcrepitant rales, persistent or transitory, heard over 
the inferior margin of the normal lung at the bottom of the axilla, 
is shown by the following figures : Out of 356 normal chests to 
which I have listened especially for these rales, I found 228, or 61 
per cent, which showed them on one or both sides. They are very 
rarely to be heard in persons under twenty years of age. After 
forty-five, on the other hand, it is unusual to find them absent. 
In my experience they are considerably more frequent in the situa- 
tion shown in Fig. 124 than in any other part of the lung, but they 
may be occasionally heard in the back or elsewhere. In view of 

! A distinction was formerly drawn between crepitant and subcrepitant 
rales, on the ground that the latter were heard during both respiratory sounds 
and the former only during inspiration, but this distinction cannot be main- 
tained and is gradually being given up. 



106 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

these facts, it seems to rue that we must recognize that it is almost 
if not quite physiological to find the finer varieties of crackling 
rales at the base of the axillae in persons over forty years old. I 
have supposed these rales to be due to a partial atelectasis result- 
ing from disease in the thin lower margin of the lungs. Such por- 
tions of the lung are ordinarily not expanded unless the respirations 
are forced and deep. This explanation would agree with the obser- 
vations of Abrams, to which I shall refer later (see below, p. 290). 

(b) Crepitant or subcrepitant rales are also to be heard in a 
certain portion of cases of pneumonia, in the very earliest stages 
and when resolution is taking place ("crepitans redux"). More 
rarely this type of rale may be heard in connection with tubercu- 
losis, infarction, or oedema of the lung. 

In certain cases of dry pleurisy there occur fine crackling 
sounds which can scarcely be differentiated from subcrepitant rales. 
I shall return to the description of them in speaking of pleural 
friction (see below, p. 271). 

(3) Musical Rales. 

The passage of air through bronchial tubes narrowed by in- 
flammatory swelling of their lining membrane (bronchitis), gives 
rise not infrequently to a multitude of musical sounds. Such a 
stenosis occurring in relatively large bronchial tubes produces a 
deep-toned groaning sound, while narrowing of the finer tubes re- 
sults in piping, squeaking, whistling noises of various qualities. 
Such sounds are often known as " dry rales " in contradistinction 
to the " bubbling rales " above described, but as many non -musical 
crackling rales have also a very dry sound, it seems to me best to 
apply the more distinctive term " musical rales " to all adventitious 
sounds of distinctly musical quality which are produced in the 
bronchi. Musical rales are of all adventitious sounds the easiest 
to recognize but also the most fugitive and changeable. They ap- 
pear now here, now there, shifting from minute to minute, and may 
totally disappear from the chest and reappear again within a very 
short time. This is to some extent true of all varieties of rales, 
but especially of the squeaking and groaning varieties. 



AUSCULTATION. 107 

Musical rales are heard, as a rule, more distinctly during expira- 
tion, especially when they occur in connection with asthma or em- 
physema. In these diseases one may hear quite complicated chords 
from the combinations of rales which vary in pitch. 

VII. The Effects of Cough. 

The influence of coughing upon rales is usually very marked. 
Its effect may be either to intensify them and bring them out where 
they have not previously been heard, or to clear them away alto- 
gether. Other effects of coughing upon physical signs will be 
mentioned later on in the chapters on Pneumonia and Phthisis. 

VIII. Pleural Friction. 

The surfaces of the healthy pleural cavity are lubricated with 
sufficient serum to make them pass noiselessly over each other dur- 
ing the movements of respiration. But when the tissues become 
abnormally dry, as in Asiatic cholera, or when the serous surfaces 
are roughened by the presence of a fibrinous exudation, as in ordi- 
nary pleurisy, the rubbing of the two pleural surfaces against one 
another produces peculiar and very characteristic sounds known as 
"pleural friction sounds." The favorite seat of pleural friction 
sounds is at the bottom of the axilla, i.e., where the lung makes 
the widest excursion and where the costal and diaphragmatic pleura 
are in close apposition (see Fig. 33). In some cases pleural fric- 
tion sounds are to be heard altogether below the level of the lung. 
In others they may extend up several inches above its lower mar- 
gin, and occasionally it happens that friction may be appreciated 
over the whole lung from the top to the bottom. Very rarely 
friction sounds are heard only at the apex of the lung in early 
tuberculosis. 

The sound of pleural friction may be closely imitated by hold- 
ing the thumb and forefinger close to the ear, and rubbing them 
past each other with strong pressure, or by pressing the palm of 
one hand over the ear and rubbing upon the back of this hand with 



108 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

the fingers of the other. Pleural friction is usually a catchy, 
jerky, interrupted, irregular sound, and is apt to occur during in- 
spiration only, and particularly at the end of this act. It may, 
however, be heard with both respiratory acts, but rarely if ever 
occurs during expiration alone. The intensity and quality of the 
sounds vary a great deal, so that they may be compared to grazing, 
rubbing, rasping, and creaking sounds. They are sometimes spoken 
of as " leathery." As a rule, they seem very near to the ear, and are 
sometimes startlingly loud. In many cases they cannot be heard 
after the patient has taken a few full breaths, probably because the 
rough pleural surfaces are smoothed down temporarily by the fric- 
tion which deep breathing produces. After a short rest, however, 
and a period of superficial breathing, pleural friction sounds often 
return and can be heard for a short time with all their former in- 
tensity. They are increased by pressure exerted upon the outside 
of the chest wall. Such pressure had best be made with the hand 
or with the Bowles stethoscope, since the sharp edges of the chest- 
piece of the ordinary stethoscope may give rise to considerable 
pain ; but if such pressure is made with the hand, one must be 
careful not to let the hand shift its position upon the skin, else 
rubbing sounds may thus be produced which perfectly simulate 
pleural friction. In well-marked cases pleuritic friction can be 
felt if the palm of the hand is laid over the suspected area; occa- 
sionally the sound is so loud that it can be heard by the patient 
himself or by those around him. 

In doubtful cases, or when a friction sound appears to have 
disappeared, and when one wishes to bring it out again, there are 
several manoeuvres suggested by Abrams for obtaining this end. 

(a) The Arm Manoeuvre. 

The patient suspends respiration altogether, and the arm upon 
the affected side is raised over the head by the patient himself or 
by the physician, as in performing Sylvester's method of artificial 
respiration . During this movement we listen over the suspected area. 
" By this manoeuvre the movement of the parietal against the vis- 
ceral pleura is opposite in direction to that occurring during the 



AUSCULTATION. 109 

respiratory act, and for this reason the pleuritic sound may often 
be elicited after it has been exhausted in the ordinary act of breath- 
ing." 

(b) The Decubital Manoeuvre. 

" Let the patient lie upon the affected side for a minute or two, 
then let him rise quickly and suspend respiration. Now listen over 
the affected area, at the same time directing the patient to take a 
deep breath." 

Pleuritic friction sounds are distinguished from rales by their 
greater superficiality, by their jerky, interrupted character, by the 
fact that they are but little influenced by cough, and that they are 
increased by pressure. It has already been mentioned, however, 
that there is one variety of sounds which we have every reason to 
think originate in the pleura, which cannot be distinguished from 
certain varieties of crackling bronchial rales. Such sounds occur 
chiefly in connection with phthisical processes, in which both pleu- 
risy and bronchitis are almost invariably present, and it is seldom 
of importance to distinguish the two. 

IX. Auscultation of the Spoken or Whispered Voice Sounds. 
The more important of these is : 

(a) The Whispered Voice. 

The patient is directed to whisper "one, two, three," or 
"ninety -nine," while the auscultator listens over different portions 
of the chest to see to what degree the whispered syllables are trans- 
mitted. In the great majority of normal chests the whispered 
voice is to be heard only over the trachea and primary bronchi in 
front and behind, while over the remaining portions of the lung 
little or no sound is to be heard. When, on the other hand, solidi- 
fication of the lung is present, the whispered voice may be dis- 
tinctly heard over portions of the lung relatively distant from the 
trachea and bronchi ; for example, over the lower lobes of the lung 
behind. The usefulness of the whispered voice in the search for 
small areas of solidification or for the exact boundaries of a solidi- 



110 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

fied area is very great, especially when we desire to save the patient 
the pain and fatigne of taking deep breaths. Whispered voice 
sounds are practically equivalent to a forced expiration and can be 
obtained with very little exertion on the patient's part. The in- 
creased transmission of the whispered voice is, in my opinion, a 
more delicate test for solidification than tubular breathing. The 
latter sign is present only when a considerable area of lung tissue 
is solidified, while the increase of the whispered voice may be ob- 
tained over much smaller areai. Eetraction of the lung above the 
level of a pleural effusion causes a moderate increase in the trans- 
mission of the whispered voice, and at times this increased or bron- 
chial whisper is to be heard over the fluid itself, probably by trans- 
mission from the compressed lung above. 

Where the lung is completely solidified the whispered words 
may be clearly distinguished over the affected area. In lesser de- 
grees of solidification the syllables are more or less blurred. 

(b) The Spoken Voice. 

The evidence given us by listening for the spoken voice in vari- 
ous parts of the chest is considerably less in value than that obtained 
through the whispered voice. As a rule, it corresponds with the 
tactile fremitus, being increased in intensity by the same causes 
which increase tactile fremitus, viz., solidification or condensation 
of the lung, and decreased by the same causes which decrease tac- 
tile fremitus — namely, by the presence of air or water in the pleu- 
ral cavity, by the thickening of the pleura itself, or by an. ob- 
struction of the bronchus leading to the part over which we are 
listening. In some cases the presence of solidification of the lung 
gives rise not merely to an increase in transmission of the spoken 
voice, but to a change in its quality, so that it sounds abnormally 
concentrated, nasal, and near to the listener's ear. The latter 
change may be heard over areas where tactile fremitus is not in- 
creased, and even where it is diminished. "Where this change in 
the quality of the voice occurs, the actual words spoken can often 
be distinguished in a way not usually possible over either normal 
or solidified lung. "Bronchophony," or the distinct transmission 



AUSCULTATION. HI 

of audible words, and not merely of diffuse, unrecognizable voice 
sounds, is considerably commoner in the solidifications due to pneu- 
monia than in those due to phthisis; it occurs in some cases of 
pneumothorax and pulmonary cavity. 

(c) Egophony. 

Among the least important of the classical physical signs is a 
nasal or squeaky quality of the sounds which reach the observer's 
ear when the patient speaks in a natural voice. To this peculiar 
quality of voice the name of "egophony" has been given. It is 
most frequently heard in cases of moderate -sized pleuritic effusion 
just about the level of the lower angle of the scapula and in the 
vicinity of that point. Less often it is heard at the same level in 
front. It is very rarely heard in the upper portion of the chest 
and is by no means constant either in pleuritic effusion or in any 
other condition. A point at which it is heard corresponds not, as 
a rule, with the upper level of the accumulated fluid, as has been 
frequently supposed, but often with a point about an inch farther 
down. The presence of egophony is in no way distinctive of pleu- 
ritic effusions and may be heard occasionally over solidified lung. 

X. Phenomena Peculiar to Pneumohydrothorax and Pneu- 

MOPYOTHORAX. 

(1) Succussion. 

Now and then a patient consults a physician, complaining that 
he hears noises inside him as if water were being shaken about. 
One such patient expressed himself to me to the effect that he felt 
"like a half -empty bottle." In the chest of such a patient, if one 
presses the ear against any portion of the thorax and then shakes 
the whole patient strongly, one may hear loud splashing sounds 
known technically as "succussion." Such sounds are absolutely 
diagnostic of the presence of both air and fluid in the cavity over 
which they are heard. Very frequently they may be detected by 
the physician when the patient is not aware of their presence. Oc- 



112 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

casionally the splashing of the fluid within may be felt as well as 
heard. It is essential, of course, to distinguish succussion due to 
the presence of air and fluid in the pleural cavity from similar 
sounds produced in the stomach, but this is not at all difficult in 
the majority of cases. It is a bare possibility that succussion 
sounds may be due to the presence of air and fluid in the pericar- 
dial cavity. 

It is important to remember that succussion is never to be 
heard in simple pleuritic effusion or hydrothorax. The presence of 
air, as well as liquid, in the pleural cavity is absolutely essential to 
the production of succussion sounds. 1 

(2) Metallic Tinkle or Falling-Drop Sound. 

When listening over a pleural cavity which contains both air 
and fluid, one occasionally hears a liquid, tinkling sound, due pos- 
sibly to the impact of a drop of liquid falling from the relaxed 
lung above into the accumulated fluid at the bottom of the pleural 
cavity, and possibly to rales produced in the tissues around the 
cavity. It is stated that this physical sign may in rare cases be 
observed in large -sized phthisical cavities as well as in pneumohy- 
drothorax and pneumopyothorax. 

(3) The Lung-Fistula Sound. 

When a perforation of the lung occurs below the level of the 
fluid accumulated in the pleural cavity, bubbles of air may be forced 
out from the lung and up through the fluid with a sound reminding 
one of that made by children when blowing soap-bubbles. 

1 It is well for the student to try for himself the following experiment, 
which I have found useful in impressing these facts upon the attention of 
classes in physical diagnosis: Fill an ordinary rubber hot-water bag to the 
brim with water. Invert it and squeeze out forcibly a certain amount (per- 
haps half) of the contents, hy grasping the upper end of the bag and compress- 
ing it. While the water is thus being forced out, screw in the nozzle of the 
bag. Now shake the whole bag, and it will be found impossible to produce 
any splashing sounds owing to the fact that there is no air in the bag. Un- 
screw the nozzle, admit air, and then screw it in again. Now shake the bag 
again and loud splashing will be easily heard. 



CHAPTER V. 

AUSCULTATION OF THE HEART. 

I. "Valve Akeas." 

In the routine examination of the heart, most observers listen 
in four places : 

(1) At the apex of the heart in the fifth intercostal space near 
the nipple, the "mitral area." 



Aortic area. 



Tricuspid area. 




_J — Pulmonic area. 



— Mitral area. 



Fig. 75.— The Valve Areas. 

(2) In the second left intercostal space near the sternum, the 
"pulmonic area. " 

(3) In the second right intercostal space near the sternum, the 
"aortic area." 

(4) At the bottom of the sternum near the ensiform cartilage, 
the "tricuspid area." 

These points are represented in Fig. 75 and are known as 
8 



114 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

"valve areas." They do not correspond to the anatomical position 
of any one of the four valves, but experience has shown that sounds 
heard best at the apex can be proved (by post-mortem examination 
or otherwise) to be produced at the mitral orifice. Similarly sounds 
heard best in the second left intercostal space are proved to be 
produced at the pulmonary orifice ; those which are loudest at the 
second right intercostal space to be produced at the aortic orifice ; 1 
while those which are most distinct near the origin of the ensiform 
cartilage are produced at the tricuspid orifice. 

II. The Normal Heart Sounds. 

A glance at Fig, 75, which represents the anatomical positions 
of the four valves above referred to, illustrates what I said above ; 
namely, that the traditional valve areas do not correspond at all 
with the anatomical position of the valves. If now we listen in 
the "mitral area" that is, in the region of the apex impulse of the 
heart, keeping at the same time one finger on some point .at which 
the cardiac impulse is palpable, one hears with each outward thrust 
of the heart a low, dull sound, and in the period between the heart 
beats a second sound, shorter and sharper in quality. 2 

That which occurs with the cardiac impulse is known as the 
first sound ; that which occurs between each two beats of the heart 
is known as the second sound. The second sound is generally ad- 
mitted to be due to the closure of the semilunar valves The cause 
of the first sound has been a most fruitful source of discussion, and 
no one explanation of it can be said to be generally received. Per- 
haps the most commonly accepted view attributes the first or 
systolic sound of the heart to a combination of two elements — 

(a) The contraction of the heart muscle itself. 

(b) The sudden tautening of the mitral curtains. 

Following the second sound there is a pause corresponding to 

1 For exceptions to this rule, see below, page 176. 

2 The first sound of the heart, as heard at the apex, may be imitated by- 
holding a linen handkerchief by the corners and suddenly tautening one of the 
borders. To imitate the second sound, use one-half the length of the border 
instead of the whole. 



AUSCULTATION OF THE HEART. 



115 



the diastole of the heart. Normally this pause occupies a little 
more time than the first and second sounds of the heart taken to- 
gether. In disease it may be much shortened. 

The first sound of the heart is not only longer and duller than 
the second (it is often spoken of as " booming " in contrast with the 
" snapping " quality of the second sound) but is also considerably 
more intense, so that it gives us the impression of being accented 
like the first syllable of a trochaic rhythm. After a little practice 
one grows so accustomed to this rhythm that one is apt to rely upon 



„.- Aortic valve. 
Pulmonic valve. 



Tricuspid valve. 




Mitral valve. 



/ 

Fig. 76.— Anatomical Position of the Cardiac Valves. 



his appreciation of the rhythm alone for the identification of the 
systolic sound. This is, however, an unsafe practice and leads to 
many errors, Our impression as to which of the two sounds of each 
cardiac cycle corresponds to systole should always be verified either 
by sight or touch. We must either see or feel the cardiac impulse 
and assure ourselves that it is synchronous with the heart sound 
which we take to be systolic. 1 This point is of especial importance 
in the recognition and identification of cardiac murmurs, as will be 
seen presently. 

1 When the cardiac impulse can be neither seen nor felt, the pulsation of 
the carotid will generally guide us. The radial pulse is not a safe guide. 



116 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

So far, I have been describing the normal heart sounds heard 
in the "mitral area," that is, at the apex of the heart. If now we 
listen over the pulmonary area (in the second left intercostal 
space), we find that the rhythm of the heart sounds has changed 
and that here the stress seems to fall upon the "second sound," 
i.e., that corresponding to the beginning of diastole; in other 
words, the first sound of the heart is here heard more feebly and 
the second sound more distinctly. The sharp, snapping quality of 
the latter is here even more marked than at the apex, and despite 
the feebleness of the first sound in this area we can usually recog- 
nize its relatively dull and prolonged quality. 

Over the aortic area (i.e., in the second right interspace) the 
rhythm is the same as in the pulmonary area, although the second 
sound may be either stronger or weaker than the corresponding 
sound on the other side of the sternum (see below, p. 118). 

Over the tricuspid area one hears sounds practically indistin- 
guishable in quality and in rhythm from those heard at the apex. 

When the chest walls are thick and the cardiac sounds feeble, 
it may be difficult to hear them at all. In such cases the heart 
sounds may be heard much more distinctly if the patient leans for- 
ward and toward his own left so as to bring the heart closer to the 
front of the chest. Such a position of the body also renders it 
easier to map out the outlines of the cardiac dulness by percussion. 

In cardiac neuroses and during conditions of excitement or emo- 
tional strain, the first sound at the apex is not only very loud but 
has often a curious metallic reverberation (" cliquetis metallique ") 
corresponding to the trembling, jarring cardiac impulse (often mis- 
taken for a thrill) which palpation reveals. 

III. Modifications in the Intensity of the Heart Sounds. 

It has already been mentioned that in young persons with thin, 
elastic chests, the heart sounds are heard with greater intensity 
than in older persons whose chest walls are thicker and stiller. 
In obese, indolent adults it is sometimes difficult to hear any heart 
sounds at all, Avhile in young persons of excitable temperament the 
sounds may have a very intense and ringing quality. Under dis- 



AUSCULTATION OF THE HEART. 117 

eased conditions either of the heart sounds may be increased or 
diminished in intensity. I shall consider 

(1) The First Sound at the Apex [sometimes Called the Mitral First 

Sound) 

(a) Increase in the length or intensity of the first sound at the 
apex of the heart occurs in any condition which causes the heart 
to act with unusual degree of force, such as bodily or mental exer- 
tion, or excitement. In the earlier stages of infectious fevers a 
similar increase in the intensity of this sound may sometimes be 
noted. Hypertrophy of the left ventricle sometimes has a similar 
effect upon the sound, but less often than one would suppose, while 
dilatation of the left ventricle, contrary to what one would suppose, 
is not infrequently associated with a loud, forcible first sound at 
the apex. In mitral stenosis the first sound is usually very intense 
and is often spoken of as a " thumping first sound " or as a " sharp 
slap." 

(b) Shortening and weakening of the first sound at the apex. 
In the course of continued fevers and especially in typhoid fever 

the granular degeneration which takes place in the heart muscle is 
manifested by a shortening and weakening of the first sound at the 
apex, so that the two heart sounds come to seem much more alike 
than usual. In the later stages of typhoid, the first sound may 
become almost inaudible. The sharp "valvular " quality, which 
one notices in the first apex sound under these conditions, has been 
attributed to the fact that weakening of the myocardium has caused 
a suppression of one of the two elements which go to make up the 
first sound, namely, the muscular element, so that we hear only the 
short, sharp sound due to the tautening of the mitral curtains. 
Chronic myocarditis, or any other change in the heart wall which 
tends to enfeeble it, produces a weakening and shortening of the 
first sound similar to that just describedo Simple weakness in the 
mitral first sound without any change in its duration or pitch may 
be due to fatty overgrowth of the heart, to emphysema or pericar- 
dial effusion in case the heart is covered by the distended lung or 
by the accumulated fluid. Among valvular diseases of the heart 



118 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

the one most likely to be associated with, a diminution in intensity 
of the first apex sound is mitral regurgitation. 

(c) Doubling of the first sound at the apex. 

It is not uncommon in healthy hearts to hear in the region of 
the apex impulse a doubling of the first sound so that it may be 
suggested by pronouncing the syllables "turrupp " or "trupp." In 
health this is especially apt to occur at the end of expiration. In 
disease it is associated with many different conditions involving an 
increase in the work of one or the other side of the heart. It 
seems, however, to be unusually frequent in myocarditis. 

(2) Modifications in the Second Sounds as Heard at the Base of the 

Heart. 

Physiological Variations. — The relative intensity of the pul- 
monic second sound, when compared with the second sound heard 
in the conventional aortic area, varies a great deal at different pe- 
riods of life. Attention was first called to this by Vierordt, 1 and 
it has of late years been recognized by the best authorities on dis- 
eases of the heart, though the majority of current text -books still 
repeat the mistaken statement that the aortic second sound is always 
louder than the pulmonic second in health. 

The work of Dr. Sarah R. Creighton, done in my clinic during 
the summer of 1899, showed that in 90 per cent of healthy chil- 
dren under ten years of age, the pulmonic second sound is louder 
than the aortic. In the next decade (from the tenth to the twen- 
tieth year) the pulmonic second sound is louder in two-thirds of 
the cases. About half of 207 cases, between the ages of twenty and 
twenty-nine, showed an accentuation of the pulmonic second, while 
after the thirtieth year the number of cases showing such accentua- 
tion became smaller with each decade, until after the sixtieth year 
we found an accentuation of the aortic second in sixty-six out of sixty- 
eight cases examined. These facts are exhibited in tabular form in 

1 Vierordt: "Die Messung der Intensitat der Herztone" (Tubingen, 
1885). See also Hochsinger, "Die Auscultation des Mndlichen Herzens" ; 
Gibson, "Diseases of the Heart" (1898) ; Rosenbach, "Diseases of the Heart" 
(1900) ; Allbutt, "System of Medicine." 



AUSCULTATION OF THE HEART 



119 



Figs. 77 and 78, and appear to show that the relative intensity of 
the two sounds in the aortic and pulmonic arteries depends pri- 
marily upon the age of the individual, the pulmonic sound predomi- 
nating in youth and the aortic in old age, while in the period of 
middle life there is relatively little discrepancy between the two. 



Fig. T< 



100 



DECADES. 
10-19 | 20-29 1 30-39 | 40-49 j 50-59 j 60-69 j 70-79; 




-Showing the Per Cent of Accentuated Pulmonic Second Sound in Each Decade. 
Based on 1,000 cases. 



It is, therefore, far from true to suppose that we can obtain evi- 
dence of a pathological increase in the intensity of either of the 
second sounds at the base of the heart simply by comparing it with 
the other. Pathological accentuation of the pulmonic second 
sound must mean a greater loudness of this sound than should 
be expected at the age of the patient in question, and not simply a 
greater intensity than that of the aortic second sound. The same 



120 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

observation obviously applies^ to accentuation of the aortic second 
sound. 

Both the aortic and the pulmonic second sounds are sometimes 

DECADES. 



-90% 
-80% 

~<o% 

-60% 
-50% 

-40% 

-30% 

—20% 

10 % 



Fig. 78.— Showing the Per Cent of Accentuated Pulmonic Second Sound in Each Decade. 

Based on 1,000 cases. 

very intense during great emotional excitement or after muscular 
exertion, and sometimes without any obvious cause. 



too 5^- - 


| 0-9 


' 10-19 


20-29 


i 30-39 


| 40-49 


50-59 


60-69 


j 70-79 




QO^-- 




















80 °X— 




















70%- 






































m 

o 
m 




















> 



m 




















30%- 
20%— 
10%- 











































































Path ological Variations. 

A. Accentuation of the Pulmonic Second Sound. 

Pathological accentuation of the second sound occurs especially 
in conditions involving a backing up of blood in the lungs, such as 
occurs in stenosis or insufficiency of the mitral valve, or in obstruc- 



AUSCULTATION OF THE HEART. 121 

tive disease of the lungs (emphysema, bronchitis, phthisis, chronic 
interstitial pneumonia). Indirectly accentuation of the pulmonic 
second sound points to hypertrophy of the right ventricle, since 
without such hypertrophy the work of driving the blood through 
the obstructed lung could not long be performed. If the right ven- 
tricle becomes weakened, the accentuation of the pulmonic second 
sound is no longer heard. 

B. Weakening of the Pulmonic Second Sound. 

"Weakening of the pulmonic second sound is a very serious symp- 
tom, sometimes to be observed in cases of pneumonia or cardiac 
disease near the fatal termination. It is thus a very important 
indication for prognosis, and is to be watched for with the greatest 
attention in such cases. 

C. Accentuation of the Aortic Second Sound. 

I have already shown that the aortic second sound is louder 
than the corresponding sound in the pulmonary area in almost every 
individual over sixty years of age and in most of those over forty. 
A still greater intensity of the aortic second sound occurs — 

(a) In interstitial nephritis or any other condition which in- 
creases arterial tension and so throws an increased amount of work 
upon the left ventricle. Indirectly, therefore, a pathologically loud 
aortic sound points directly to increased tension in the peripheral 
arteries and indirectly to hypertrophy of the left ventricle. 

(b) A similar increase in the intensity of the aortic second 
sound occurs in aneurism or diffuse dilatation of the aortic arch. 

D. Diminution in the Intensity of the Aortic Second Sound. 

Whenever the amount of blood thrown into the aorta by the 
contraction of the left ventricle is diminished, as is the case espe- 
cially in mitral stenosis and to a lesser degree in mitral regurgita- 
tion, the aortic second sound is weakened so that at the apex it 
may be inaudible. A similar effect is produced by any disease 
which weakens the walls of the left ventricle, such as fibrous myo- 



122 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

carditis, fatty degeneration, and cloudy swelling. Relaxation of 
the peripheral arteries has the same effect. In conditions of col- 
lapse the aortic second sound may be almost or quite inaudible. 

In persons past middle life the second sounds are often louder 
in the third or fourth interspace than in the second, so that if we 
listen only in the second space we may gain the false impression that 
the second sounds are feeble. 

Accentuation of both the second sounds at the base of the 
heart may occur in health from nervous causes or when the lungs 
are retracted by disease so as to uncover the conus arteriosus and 
the aortic arch. Under these conditions the second sound may be 
seen and felt as welLas heard. In a similar way, an apparent in- 
crease in the intensity of either one of the second sounds at the. 
base of the heart may be produced by a retraction of one or the 
other lung. 

Summary. — (1) The mitral first sound is increased by hyper- 
trophy or dilatation of the left ventricle, and among valvular dis- 
eases especially by mitral stenosis. It is weakened or reduplicated 
by parietal disease of the heart. Any of these changes may occur 
temporarily from physiological causes. 

(2) The pulmonic second sound is usually more intense than 
the aortic in children and up to early adult life. Later the aortic 
second sound predominates. Pathological accentuation of the sec- 
ond pulmonic sound usually points to obstruction in the pulmonary 
circulation (mitral disease, emphysema, etc.). Weakening of the 
pulmonic second means failure of the right ventricle and is serious. 

(3) The aortic second sound is increased pathologically by any 
cause which increases the work of the left ventricle (arteriosclero- 
sis, chronic nephritis). It is diminished when the blood . stream, 
thrown into the aorta by the left ventricle, is abnormally small 
(mitral disease, cardiac failure). 

(4) Changes in the tricuspid sounds are rarely recognizable, 
while changes in the first aortic and pulmonic sounds have little 
practical significance. 



AUSCULTATION OF THE HEART 123 

Modifications in the Rhythm of the Cardiac Soimds. 

(1) Whenever the walls of the heart are greatly weakened by 
disease, for example, in the later weeks of a case of typhoid 
fever, the diastolic pause of the heart is shortened so that the car- 
diac sounds follow each other almost as regularly as the ticking of 
a clock; hence the term " tick-tack heart." As this rhythm is not 
unlike that heard in the foetal heart, the name of " embryocardia " 
is sometimes applied to it. The " tick-tack " rhythm may be heard 
in any form of cardiac disease after compensation has failed, or in 
any condition leading to collapse. 

(2) A less common change of rhythm is that produced by a 
shortening of the interval between the two heart sounds owing to 
an incompleteness of the contraction of the ventricle. This change 
may occur in any disease of the heart when compensation fails. 

(3) The " Gallop Rhythm." — Shortening of the diastolic pause 
together with doubling of one or another of the cardiac sounds re- 
sults in our hearing at the apex of the heart three sounds instead 
of two, which follow each other in a rhythm suggesting the hoof 
beats of a galloping horse. Such a rhythm may occur temporarily in 
any heart which is excited or overworked from any cause, but when 
permanent is usually a sign of grave cardiac weakness. The rhythms 
so produced are usually anapaestic, ^ w — ', w w — ', ww — ', or of 
this type : w — ' w, w — ' w ? s^ — ' w. 

Doubling of the Second Sounds at the Base of the Heart. — At 
the end of a long inspiration this change may be observed in al- 
most any healthy person if one listens at the base of the heart. It 
is still better brought out after muscular exertion or by holding the 
breath. In such cases it probably expresses the non-synchronous 
closure of the aortic and pulmonic valves, owing to increased press- 
ure in the pulmonary circulation. Similarly in diseased condi- 
tions, anything which increases the pressure either in the periph- 
eral arteries or in the pulmonary circulation, and thus throws 
increased work upon one or the other ventricle, will cause a doub- 
ling of the second sound as heard at the base of the heart. 

In mitral stenosis a double diastolic sound is usually to be 



124 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

heard at the apex, and in the diagnosis of this disease this " double 
shock sound n during diastole may be an important piece of evi- 
dence, and may sometimes be felt as well as heard. The " double 
shock sound " of mitral stenosis is not generally believed to repre- 
sent a doubling of the ordinary second sound, although it corre- 
sponds with diastole. Just what its mechanism is, is disputed. 

I have said nothing about modifications in the second sound at 
the apex, since this sound is now generally agreed to represent the 
aortic second sound transmitted by the left ventricle to the apex. 
The first sounds at the base of the heart have also not been dwelt 
upon, since they have no special importance in diagnosis. 

Metallic Heart Sounds. 

The presence of air in the immediate vicinity of the heart, 
as, for example, in pneumothorax or in gaseous distention of the 
stomach or intestine, may impart to the heart sounds a curious 
metallic quality such as is not heard under any other conditions. 

"Muffling," "Prolongation," or " Unclearness" of the Heart Sounds. 

These terms are not infrequently met with in literature, but 
their use should, I think, be discontinued. The facts to which 
they refer should be explained either as faintness of the heart 
sounds, due to the causes above assigned, or as faint, short mur- 
murs. In their present usage such terms as " muffled n or " unclear " 
heart sounds represent chiefly an unclearness in the mind of the 
observer as to just what it is that he hears, and not any one recog- 
nized pathological condition in the heart. 

IV. Souxds Audible Over the Peripheral Vessels. 

(1) The normal heart sounds are in adults audible over the 
carotids and over the subclavian arteries. In childhood and youth 
only the second heart sound is thus audible. 

(2) In about 7 per cent of normal persons a systolic sound can 
be heard over the femoral artery. This sound is obviously not 



AUSCULTATION OF THE HEART 125 

transmitted from the heart, and is usually explained as a result of 
the sudden systolic tautening of the arterial wall. 

In aortic regurgitation this arterial sound is almost always 
audible not only in the femoral but in the brachial and even in the 
radial, and its intensity over the femoral becomes so great that the 
term " pistol-shot " sound has been applied to it. In fevers, 
exophthalmic goitre, lead poisoning, and other diseases, a similar 
arterial sound is to be heard much more frequently than in health. 

Venous Sounds. 

The violent closure of the venous valves in the jugular is some- 
times audible in cases of insufficiency of the tricuspid valve. The 
found has no clinical importance, and is difficult to distinguish owing 
to the presence of the carotid first sound mentioned above. 



CHAPTEE VI. 

AUSCULTATION OF THE HEAET : CONTINUED. 

Cardiac Murmurs. 

(a) Terminology. 

The word " murmur " is one of the most unfortunate of all the 
terms used in the description of physical signs. No one of the 
various blowing, whistling, rolling, rumbling, or piping noises to 
which the term refers, sounds anything like a "murmur" in the 
ordinary sense of the word. Nevertheless, it does not seem best 
to try to replace it by any other term. The French word " souffle " 
is much more accurate and has become to some extent Anglicized. 
Under the head of cardiac murmurs are included all abnormal 
sounds produced within the heart itself. Pericardial friction 
sounds and those produced in that portion of the lung or pleura 
which overlies the heart are not considered "murmurs." 

(b) Mode of Production. 

With rare exceptions all cardiac murmurs are produced at or 
near one of the valve orifices, either by disease of the valves them- 
selves resulting in shrivelling, thickening, stiffening, and narrowing 
of the valve curtains, or by a stretching of the orifice into which 
the valves are inserted. 

Diseases of the valves themselves may lead to the production of 
murmurs : 

(a) When the valves fail to close at the proper time (incompe- 
tence, insufficiency, or regurgitation). 

(b) When the valves fail to open at the proper time (stenosis 
or obstruction) . 



AUSCULTATION OF THE HEART. 127 

(c) When the surfaces of the valves or of the parts immedi- 
ately adjacent are roughened so as to prevent the smooth flow of the 
blood over them. 

(d) When the orifice which the valves are meant to close is di- 
lated as a result of dilatation of the heart chamber of which it forms 





Fig. 79.— Diagram to Illustrate the Production of a Cardiac Murmur Through Regurgitation 
from the Aorta or in an Aneurismal Sac. The arrow shows the direction of the blood cur- 
rent and the curled lines the audible blood eddies. 

the entrance or exit. The valves themselves cannot enlarge to 
keep pace with the enlargement of the orifice, and hence no longer 
suffice to reach across it. 

The presence of any one of these lesions gives rise to eddies 
in the blood current and thereby to the abnormal sounds to which 
we give the name murmurs. 1 (See Figs. 79, 80, and 81). When 




o ■ 



Fig. 80.— Diagram to Illustrate the Production of a Cardiac Murmur Through Stenosis of a 

Valve-Orifice. 

valves fail to close and so allow the blood to pass back through 
them, we speak of the lesion as regurgitation, insufficiency, or in- 
competence ; if, for example, the aortic valves fail to close after 
the left ventricle has thrown a column of blood into the aorta, 
some of this blood regurgitates through these valves into the ven- 

1 The method by which functional murmurs are produced will be discussed 
later. (See page 136.) 



128 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

tricle from which it has just been expelled, and we speak of the 
lesion as "aortic regurgitation,'''' and of the murmur so produced as 
an aortic regurgitant murmur or a murmur of aortic regurgitation. 
A similar regurgitation from the left ventricle into the left auricle 
takes place in case the mitral valve fails to close at the beginning 
of systole. If, on the other hand, the mitral valve fails to open 
properly to admit the blood which should flow during diastole from 
the left auricle into the left ventricle, we speak of the condition as 
mitral stenosis or mitral obstruction. A similar narrowing of the 
aortic valves such as to hinder the egress of blood during the systole 
of the left ventricle is known as aortic stenosis or obstruction. Val- 




Fin. 81.— Diagram to Illustrate the Production of Cardiac Murmurs Through Roughening of a 

Valve. 

vular lesions of the right side of the heart (tricuspid and pulmonic 
valves) are comparatively rare, but are produced and named hi a 
way similar to those just described. 

The facts most important to know about a murmur are : 

(1) Its place in the cardiac cycle. 

(2) Its point of maximum intensity. 

(3) The area over which it can be heard. 

(4) The effects of exertion, respiration, or position upon it. 
Less important than the above are : 

(5) Its intensity. 

(6) Its quality. 

(7) Its length. 

(8) Its relation to the normal sounds of the heart- 
Each of these points will now be taken up in detail : 

(1) Time of Murmurs. — The first and most important thing to 
ascertain regarding a murmur is its relation to the normal cardiac 
cycle ; that is, whether it occurs during systole or during diastole, 
or in case it does not fill the whole of one of those periods, in what 



AUSCULTATION OF THE HEART. 129 

part of systole or diastole it occurs. It must be borne in mind that 
the period of systole is considered as lasting from the beginning of 
the first sound of the heart up to the occurrence of the second 
sound, while diastole lasts from the beginning of the second sound 
until the beginning of the first sound in the next cycle. Any mur- 
mur occurring with the first sound of the heart, or at the time when 
the first sound should take place, or in any part of the period inter- 
vening between the first sound and the second, is held to be systolic. 
Murmurs which distinctly follow the first sound or do not begin 
until the first sound is ended are known as late systolic murmurs. 

On the other hand, it seems best, for reasons to be discussed 
more in detail later on, not to give the name of diastolic to all 
murmurs which occur within the diastolic period as above defined. 
Murmurs which occur during the last part of diastole and which 
run up to the first sound of the next cycle are usually known as 
"presystolic " murmurs. All other murmurs occurring during dias- 
tole are known as diastolic. 

The commonest of all the errors in the diagnosis of disease of 
the heart is to mistake systole for diastole, and thereby to misin- 
terpret the significance of a murmur heard during those periods. 
This mistake would never happen if we were always careful to 
make sure, by means of sight or touch, just when the systole of 
the heart occurs. This may be done by keeping one finger upon 
the apex impulse of the heart or upon the carotid artery while 
listening for murmurs, or, in case the apex impulse or the pulsa- 
tions of the carotid are better seen than felt, we can control by the 
eye the impressions gained by listening. It is never safe to trust 
our appreciation of the cardiac rhythm to tell us which is the first 
heart sound and which the second. The proof of this statement 
is given by the numberless mistakes made through disregarding it. 
Equally untrustworthy as a guide to the time of systole and dias- 
tole is the radial pulse, which follows the cardiac systole at an 
interval just long enough to mar our calculations. 

(2) Localizations of Murmurs. — To localize a murmur is to find 
its point of maximum intensity, and this is of the greatest impor- 
tance in diagnosis. Long experience has shown that murmurs 
9 



130 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

heard loudest in the region of the apex beat (whether this is in the 
normal situation or displaced), are in the vast majority of cases pro- 
duced at the mitral valve. In about five per cent of the cases mitral 
murmurs may be best heard at a point midway between the position 
of the normal cardiac impulse and the ensiform cartilage, or (very 
rarely) an inch or two above this situation. 

Murmurs heard most loudly in the second left intercostal space 
are almost invariably produced at the pulmonic orifice or just above 
it in the conus arteriosus. 

Murmurs whose maximum intensity is at the root of the ensi- 
form cartilage or within a radius of an inch and a half from this 
point are usually produced at the tricuspid orifice. Murmurs pro- 
duced at the aortic orifice may be heard best in the aortic area, but 
in a large proportion of cases are loudest on the other side of the 
sternum at or about the situation of the fourth left costal cartilage. 
Occasionally they are best heard at the apex of the heart or over 
the lower part of the sternum (see above, Fig. 103). 

(3) Transmission of Murmurs. — If a murmur is audible over sev- 
eral valve areas, the questions naturally arise: "How are we to 
know whether we are dealing with a single valve lesion or with 
several? Is this one murmur or two or three murmurs? " Obvi- 
ously the question can be asked only in case the murmur which we 
find audible in various places occupies everywhere the same time 
in the cardiac cycle. It must, for example, be everywhere systolic 
or everywhere diastolic. A systolic murmur at the apex cannot 
be supposed to point to the same lesion as a diastolic murmur, no 
matter where the latter is heard. But if we hear a systolic mur- 
mur in various parts of the chest, say over the aortic, mitral, and 
tricuspid regions, how are we to know whether the sound is simple 
or compound, whether produced at one valve orifice or at several? 

This question is sometimes difficult to answer, and in a given 
case skilled observers may differ in their verdict, but, as a rule, the 
difficulty may be overcome as follows : 

(1) Experience and post-mortem examination have shown that 
the murmur produced by each of the valvular lesions has its own 
characteristic area of propagation, over which it is heard with an in- 



AUSCULTATION OF THE HEART. 



131 



tensity which, regularly diminishes as we recede from a maximum 
whose seat corresponds with some one of the valve areas just de- 
scribed. These areas of propagation are shown in Figs. 91, 92, 95, 
and 100. Any murmur whose distribution does not extend beyond 
one of these areas, and which steadily and progressively diminishes 
in intensity as we move away from the valve area over which it is 
loudest, may be assumed to be due to a single valve lesion and no 




Fig. 82.— Mitral and Tricuspid Regurgitation. The intensity of the systolic murmur is least at 
the " waist " of the shaded area and increases as one approaches either end of it. 



more. Provided but one valve is diseased, this course of procedure 
gives satisfactory results. 

(2) When several valves are diseased and several murmurs may 
be expected, it is best to start at some one valve area, say in the 
mitral or apex region, and move the stethoscope one-half an inch 
at a time toward one of the other valve areas, noting the intensity 
of any murmur we may hear at each of the different points passed 
over. As we move toward the tricuspid area, we may get an im- 
pression best expressed by Fig. 82. That is, a systolic murmur 
heard loudly at the apex may fade away as we move toward the 
ensiform, until at the point x (Fig. 82) it is almost inaudible. But 
as we go on in the same direction the murmur may begin to grow 



132 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

louder (and perhaps to change in pitch and quality as well) until a 
maximum is reached at the tricuspid area, beyond which the mur- 
mur again fades out. 

These facts justify us in suspecting that we are dealing with two 
murmurs, one produced at the tricuspid and one at the mitral ori- 
fice. The suspicion is more likely to be correct if there has been 
a change in the pitch and quality of the murmur as we n eared the 
tricuspid orifice, and may be confirmed by the discovery of other 
evidences of a double lesion. No diagnosis is satisfactory which 
rests on the evidence of murmurs alone. Changes in the size of 
the heart's chambers or in the pulmonary or peripheral circulations 
are the most important facts in the case. Nevertheless the effort 
to ascertain and graphically to represent the intensity of cardiac 
murmurs as one listens along the line connecting the valve areas 
has its value. An "hour-glass" murmur, such as that represented 
in Fig. 82, generally means two-valve lesions. A similar "hour- 
glass " may be found to represent the auditory facts as we move 
from the mitral to the pulmonic or to the aortic areas (see Fig. 
83), and, as in the previous case, arouses our suspicion that more 
than one valve is diseased. 

It must not be forgotten, however, that " a murmur may travel 
some distance underground and emerge with a change of quality " 
( Allbutt) . This is especially true of aortic murmurs, which are often 
heard well at the apex and at the aortic area, and faintly in the in- 
tervening space, probably owing to the interposition of the right 
ventricle. 

In such cases we must fall back upon the condition of the heart 
itself, as shown by inspection, palpation, and percussion, and upon 
the condition of the pulmonary and peripheral circulation, as 
shown in the other symptoms and signs of the cases (dropsy, cough, 
etc.). 

(4) Intensity of Murmurs. — Sometimes murmurs are so loud 
that they are audible to the patient himself or even at some dis- 
tance from the chest. In one case I was able to hear a murmur 
eight feet from the patient. Such cases are rare and usually not 
serious, for the gravity of the lesion is not at all proportional to 



AUSCULTATION OF THE HEART. 



133 



the loudness of the murmur; indeed, other things being equal, 
loud murmurs are less serious than faint ones, provided we are sure 
we are dealing with organic lesions. (On the distinction between 
the organic and functional murmurs, see below, p. 138.) 

A loud murmur means a powerful heart driving the blood 
strongly over the diseased valve. When the heart begins to fail, 
the intensity of the murmur proportionately decreases because the 
blood does not flow swiftly enough over the diseased valve to pro- 




FlG. 83.— Mitral Regurgitation and Aortic Stenosis. The systolic murmur is loudest at the ex- 
tremities of the shaded area and faintest at its 



duce as loud a sound as formerly. The gradual disappearance of 
a murmur known to be due to a valvular lesion is, therefore, a very 
grave sign, and its reappearance revives hope. Patients are not 
infrequently admitted to a hospital with valvular heart trouble 
which has gone on so long that the muscle of the heart is no longer 
strong enough to produce a murmur as it pumps the blood over the 
diseased valve. In such a case, under the influence of rest and 
cardiac tonics, one may observe the development of a murmur as 
the heart wall regains its power, and the louder the murmur be- 
comes the better the condition of the patient. On the other hand, 
when the existence of a valvular lesion has been definitely deter- 



134 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

mined, and yet the compensation remains perfectly good (for exam- 
ple, in the endocarditis occurring in children in connection with 
chorea) , an increase in the loudness of the murmur may run paral- 
lel with the advance in the valvular lesion. 

In general the most important point about the intensity of a 
murmur is its increase or decrease while under observation, and not 
its loudness at any one time. 

(5) Quality of Heart Murmurs. — It has been already mentioned 
that the quality of a heart murmur is never anything like the 
sound which we ordinarily designate by the word "murmur." The 
commonest type of heart murmur has a blowing quality, whence the 
old name of "bellows sound." The sound of the letter "f " pro- 
longed is not unlike the quality of certain murmurs. Blowing 
murmurs may be low-pitched like the sound of air passing through 
a large tube, or high-pitched approaching the sound of a whistle. 
This last type merges into that known as the musical murmur, in 
which there is a definite musical sound whose pitch can be identi- 
fied. Rasping or tearing sounds often characterize the louder 
varieties of murmurs. 

Finally, there is one type of sound which, though included 
under the general name murmur, differs entirely from, any of the 
other sounds just described. This is the "presystolic roll," which 
has a rumbling or blubbering quality or may remind one of a short 
drum-roll. This murmur is always presystolic in time and usually 
associated with obstruction at the mitral or tricuspid valves. Not 
infrequently some part of a cardiac murmur will have a musical 
quality while the rest is simply blowing or rasping in character. 
Musical murmurs do not give us evidence either of an especially 
serious or especially mild type of disease. Their chief importance 
consists in the fact that they rarely exist without some valve 
lesion, 1 and are, therefore, of use in excluding the type of mur- 
mur known as " functional '," presently to be discussed, and not 
due to valve disease. Very often rasping murmurs are associated 
either with the calcareous deposit upon a valve or very marked 
narrowing of the valve orifice. 

1 Rosenbach holds that they may be produced by adhesive pericarditis. 



AUSCULTATION OF THE HEART, 135 

Murmurs may be accented at the beginning or the end ; that is, 
they may be of the crescendo type, growing louder toward the end, 
or of the decrescendo type with their maximum intensity at the 
beginning. Almost all murmurs are of the latter type except those 
associated with mitral or tricuspid obstruction. 

(6) Length of Murmurs. — Murmurs may occupy the whole 
of systole, the whole of diastole, or only a portion of one of 
these periods, but no conclusions can be drawn as to the severity 
of the valve lesion from the length of the murmur. A short mur- 
mur, especially if diastolic, may be of very serious prognostic im- 
port. 

(7) Relations to the Normal Sounds of the Heart. — Cardiac mur- 
murs may or may not replace the normal heart sounds. They may 
occur simultaneously with one or both sounds or between the 
sounds. These facts have a certain amount of significance in prog- 
nosis. Murmurs which entirely replace cardiac sounds usually mean 
a severer disease of the affected valve than murmurs which accom- 
pany, but do not replace, the normal heart sounds. Post-systolic 
or late systolic murmurs, which occur between the first and the 
second sound, are usually associated with a relatively slight degree 
of valvular disease. Late diastolic murmurs, on the other hand, 
have no such favorable significance. 

(8) Effects of Position, Exercise, and Respiration upon Cardiac 
Murmurs. — Almost all cardiac murmurs are affected to a greater 
or less extent by the position which the patient assumes while he 
is examined. Systolic murmurs which are inaudible while the 
patient is in a sitting or standing position may be quite easily 
heard when the patient lies down. On the other hand, a pre- 
systolic roll which is easily heard when the patient is sitting up 
may entirely disappear when he lies down. Diastolic murmurs 
are relatively little affected by the position of the patient, but 
in the majority of cases are somewhat louder in the upright posi- 
tion. 

The effects of exercise may perhaps be fitly mentioned here. 
Feeble murmurs may altogether disappear when the patient is at 
rest, and under such circumstances may be made easily audible by 



136 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

getting the patient to walk briskly up and down the room a few 
times. Such lesions are usually comparatively slight. 1 On the 
other hand, murmurs which become more marked as a result of rest 
are generally of the severest type (see above, p. 132). 

Organic murmurs are usually better heard at the end of expira- 
tion and become fainter during inspiration as the expanding lung 
covers the heart. This is especially true of those produced at the 
mitral valve, and is in marked contrast with the variations of func- 
tional murmurs which are heard chiefly or exclusively at the end of 
inspiration. 

(9) Sudden Metamorphosis of Murmurs. — In acute endocarditis, 
when vegetations are rapidly forming and changing their shape 
upon the valves, murmurs may appear and disappear very sud- 
denly. This metamorphosing character of cardiac murmurs, when 
taken in connection with other physical signs, may be a very im- 
portant factor in the diagnosis of acute endocarditis. In a similar 
way relaxation or rupture of one of the tendinous cords, occurring 
in the course of acute endocarditis, may effect a very sudden change 
in the auscultatory phenomena. 

" Functional Murmurs." 

Not every murmur which is to be heard over the heart points to 
disease either in the valves or in the orifices of the heart. Perhaps 
the majority of all murmurs are thus unassociated with valvular 
disease, and to such the name of "accidental," "functional," or 
" hsemic " murmurs has been given. The origin of these " functional " 
murmurs has given rise to an immense amount of controversy, and 
ifc cannot be said that any one explanation is now generally agreed 
upon. To me the most plausible view is that which regards most 
of them as due either to a temporary or permanent dilatation of 
the conus arteriosus, or to pressure or suction exerted upon the 
overlapping lung margins by the cardiac contractions. This ex- 
plains only the systolic functional murmurs, which make up ninety- 
nine per cent, of all functional murmurs. The diastolic functional 
murmurs, which undoubtedly occur, although with exceeding rarity, 
1 For exception to this see below, page 161. 



AUSCULTATION OF THE HEART. 137 

are probably due to sounds produced in the veins of the neck and 
transmitted to the innominate or vena cava. 

Characteristics of Functional Murmurs. — (1) Almost all func- 
tional murmurs are systolic, as has before been mentioned. 

(2) The vast majority of them are heard best over the pulmonic 
valve in the second left intercostal space. From this point they 
are transmitted in all directions, and are frequently to be heard, al- 
though with less intensity, in the aortic and mitral areas. Occa- 
sionally they may have their maximum intensity in one of the latter 
positions. 

(3) As a rule, they are very soft and blowing in quality, though 
exceptionally they may be loud and rough. 

(4) They are not associated with any evidence of enlargement 
of the heart nor with accentuation of the pulmonic second sound. 1 

(5) They are usually louder at the end of inspiration. 

(6) They are usually heard over a very limited area and not 
transmitted to the left axilla or to the back. 

(7) They are especially evanescent in character ; for example, 
they may appear at the end of a hard run or boat race or during 
an attack of fever, and disappear within a few days or hours. Res- 
piration, position, and exercise produce greater variations in them 
than in " organic " murmurs. 

(8) They are especially apt to be associated with ancemia, 
although the connection between anaemia and functional heart mur- 
murs is by no means as close as has often been supposed. The 
severest types of anaemia, for example pernicious anaemia, may not 
be accompanied by any murmur, while, on the other hand, typical 
functional murmurs are often heard in patients whose blood is nor- 
mal, and even in full health. It should not be forgotten that a 
real, though temporary, leakage through the mitral or tricuspid 
valve may be associated with anaemia or debilitated conditions 
owing to weakening of the papillary muscles or of the mitral 
sphincter. In such cases we find not the -signs of a functional 

1 In chlorosis the second pulmonic sound is often very loud (owing to the 
retraction of the lungs and uncovering of the conus arteriosus) and associated 
with a systolic murmur. 



138 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

murmur, as above described, but the evidence of an organic valve 
lesion hereafter to be described. 

The distinctions between organic and functional heart murmurs 
may be summed up as follows : 

Organic murmurs may occupy any part of the cardiac cycle ; if 
systolic, they are usually transmitted either into the axilla and 
back or into the great vessels of the neck ; they are usually asso- 
ciated with evidences of cardiac enlargement and changes in the sec- 
ond sounds at the base of the heart, as well as with signs and symp- 
toms of stasis in other organs. Organic murmurs not infrequently 
have a musical or rasping quality, although this is by no means al- 
ways the case. They are rarely loudest in the pulmonic area and 
are relatively uninfluenced by respiration, position, or exercise. 

Functional murmurs are almost always systolic in time and 
usually heard with maximum intensity in the pulmonic area. They 
are rarely transmitted beyond the precordial region and are usually 
loudest at the end of inspiration. They are not accompanied by 
evidences of cardiac enlargement or pathological accentuation of 
the second sounds at the base of the heart, nor by signs of venous 
stasis or dropsy. They are very apt to be associated with anaemia 
or with some special attack upon the resources of the body (e.g., 
physical overstrain or fever), and to disappear when such forces are 
removed. They are usually soft in quality ; never musical. The 
very rare diastolic functional murmur occurs exclusively, so far as 
I am aware, in conditions of profound anaemia ; i.e. , when the haemo- 
globin is twenty-five' per cent or less. It can be abolished by press- 
ure upon the bulbus jugularis, and can be observed, if followed up 
into the neck, to pass over gradually into a continuous venous hum 
with a diastolic accent. 

Cardio- Respiratory Murmurs. 

When a portion of the free margin of the lung is fixed by ad- 
hesions in a position overlapping the heart, the cardiac movements 
may rhythmically displace the air in such piece of lung so as to 
give rise to sounds which at times closely simulate cardiac mur- 
murs. These conditions are most often to be found in the tongue- 



AUSCULTATION OF THE HEART. 139 

like projection of the left lung, which normally overlaps the heart, 
but it is probably the case that cardio-respiratory murmurs may be 
produced without any adhesion of the lung to the pericardium 
under conditions not at present understood. Such murmurs may 
be heard under the left clavicle or below the angle of the left scap- 
ula, as well as near the apex of the heart, — less often in other parts 
of the chest. 

Cardio-respiratory murmurs may be either systolic or diastolic, 
but the vast majority of cases are systolic. The area over which 
they are audible is usually a very limited one. They are greatly 
affected by position and by respiration, and are heard most distinctly 
if not exclusively during inspiration, especially at the end of that 
act. (This fact is an important aid in distinguishing them from 
true cardiac murmurs, which are almost always fainter at the end 
of inspiration.) They are also greatly affected by cough or forced 
respiration or by holding the breath, whereas cardiac murmurs 
are relatively little changed thereby. Pressure on the outside 
of the thorax and in their vicinity may greatly modify their in- 
tensity or quality, while organic cardiac murmurs are but little 
influenced by 'pressure. As a rule, they have the quality of nor- 
mal respiratory murmur, and sound like an inspiration interrupted 
by each diastole of the heart. 

In case the effect of the cardiac movements is exerted upon a 
piece of lung in which a catarrhal process is going on, we may have 
systolic or diastolic explosions of rales, or any type of respiratory 
murmur except the bronchial type, since this is produced in solid lung 
which could not be emptied or filled under the influence of the car- 
diac movements. Cardio-respiratory murmurs have no special diag- 
nostic significance, and are mentioned here only on account of the im- 
portance of not confusing them with true cardiac murmurs. They 
were formerly thought to indicate phthisis, but such is not the case. 

Murmurs of Venous Origin. 

I have already mentioned that the venous hum so often heard 
in the neck in cases of anaemia may be transmitted to the region of 
the base of the heart and heard there as a diastolic murmur owing 



140 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

to the acceleration of the venous current by the aspiration of the 
right ventricle during diastole. Such murmurs are very rare and 
may usually be obliterated by pressure upon the bulbus jugularis, 
or even by the compression brought to bear upon the veins of the 
neck when the head is sharply turned to one side. They are heard 
better in the upright position and during inspiration. 

Arterial Murmurs. 

(1) Roughening of the arch of the aorta, due to chronic endo- 
carditis, is a frequent cause in elderly men of a systolic murmur, 
heard best at the base of the heart and transmitted into the vessels 
of the neck. Such a murmur is sometimes accompanied by a pal- 
pable thrill. From cardiac murmurs it is distinguished by the lack 
of any other evidence of cardiac disease and the presence of marked 
arterio-sclerosis in the peripheral vessels (see further discussion 
under Aortic Stenosis, p. 180, and under Aneurism, p. 220). 

(2) A narrowing of the lumen of the left subclavian artery, due 
to some abnormality in its course, may give rise to a systolic mur- 
mur heard close below the left clavicle at its outer end. The mur- 
mur is greatly influenced by movements of the arm and especially 
by respiratory movements. During inspiration it is much louder, 
and at the end of a forced expiration it may disappear altogether. 
Occasionally such murmurs are transmitted through the clavicle so 
as to be audible above it. 

(3) Pressure exerted upon any of the superficial arteries (carot- 
id, femoral, etc.) produces a systolic murmur (see below, p. 178). 
Diastolic arterial murmurs are peculiar to aortic regurgitation. 

(4) Over the anterior fontanelle in infants and over the gravid 
uterus systolic murmurs are to be heard which are probably arterial 
in origin. 



PART II. 

DISEASES OF THE HEART. 



CHAPTER VII. 

VALVULAR LESIONS. 

Clixicallt it is convenient to divide the ills which befall the 
heart into three classes : 

(1) Those which deform the cardiac valves (valvular lesions). 

(2) Those which weaken the heart wall (parietal disease). 

(3) Congenital malformations. 

Lesions which affect the cardiac valves without deforming them 
are not often recognizable during life. The vegetations of acute 
endocarditis 1 do not usually produce any peculiar physical signs 
until they have so far deformed or obstructed the valves as to pre- 
vent their opening or closing properly. 

The murmurs which are often heard over the heart in cases of 
acute articular rheumatism cannot be considered as evidence of 
vegetative endocarditis unless valvular deformities, and their re- 
sults in valvular obstruction or incompetency, ensue. The chordae 
tenclineae may be ruptured or shortened, thickened, and welded to- 
gether into shapeless masses, but if these deformities do not affect 
the action of the valves we have no means of recognizing them dur- 
ing life. Congenital malformations are practically unrecognizable 
as such. If they do not affect the valves, we cannot with any cer- 
tainty make out what is wrong. 

For physical diagnosis, then, heart disease means either de- 
formed valves or weakened walls. Whatever else may exist, we 
are none the wiser for it unless the autopsy enlightens us. 

1 See Appendix. 



142 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

In this chapter I shall confine myself to the discussion of valvu- 
lar lesions and their results. 

Valvular lesions are of two types : 

(a) Those which produce partial obstruction of a valve orifice 
or prevent its opening fully ("stenosis"). 



Valvula aemilun 
sinistra a. prtlmonal 




"Valvula semilunaris 
riestra a. pnlmcmalis. 



A" 



Valvula semilunaris 
" .posterior aortao 



_}y. Cuspis 



Valvula© 
tricus- 
pidalia 



\ 


t — 


<.__-- 


\ 


/ 


/ 


\ 


/ 


...J s.^--* 


f > 


' 


\ 


y 




\ , 


,-~ 




— K" 






\ v 







Fig. 84.— The Base of the Contracted Heart Showing Sphincteric Action of the Muscular Fibres 
Surrounding the Mitral and Tricuspid Valves. The outer dotted line is the outline of the 
relaxed heart. The inner dotted circles show the size of the mitral and tricuspid valves 
during diastole, a, Outline of the heart when relaxed ; b, outline of the relaxed tricuspid 
valve ; c, outline of the mitral orifice during diastole. 



(b) Those which produce leakage through a valve orifice or 
prevent its closing effectively ("regurgitation," "insufficiency," 
11 incompetency ") . 

Stenosis results always from the stiffening, thickening, and con- 
traction of a valve. 

Kegurgitation, on the other hand, may be the result either of— 



VALVULAR LESIONS. 



143 



(«) Deformity of a valve, or 

(b) Weakening of the heart muscle. 

The mitral and tricuspid orifices are closed not simply by the 
shutting of their valves, but also in part by the sphincter-like ac- 
tion of the circular fibres of the heart wall (see Fig. 84) and the 
contraction of the papillary muscles (Fig. 85). 

In birds the tricuspid orifice has no valve and is closed wholly 
by the muscular sphincter of 
the heart wall. 

In conditions of acute car- 
diac failure, such as may oc- 
cur after a hard run, the 



Mitral curtains. 



in all 



Chordea 
tendinese. 



Papillary 

muscle. 




Circular or 

— sphincteric 
fibres. 

— Endocardium. 



Myocardium. 



— Pericardium. 



papillary muscles are 
probability relaxed, 
so that the valve -flaps 
swing back into the 
auricle and permit re- 
gurgitation of blood 
from the ventricle. 

Valvular incom- 
petence, then, differs from 
valvular obstruction in that 
the latter always involves 
deformity and stiffening of 
valves, while incompetence 
or leakage is often the result 
of deficient muscular action 

on the part of the heart wall. An obstructed valve is almost always 
leaky as well, since the same deformities which prevent a valve 
from opening usually prevent its closure; but this rule does not 
work backward. A leaky valve is often not obstructed. It is leaky 
but not obstructed if the valve curtain has been practically de- 
stroyed by endocarditis; or, again, it is leaky but not obstructed if 
the leak represents muscular weakening of the mitral sphincter or 
of the papillary muscles. Pure stenosis is very rare. Pure regur- 
gitation is very common. 



Fig. 85. -The Mitral Valve Closed, Showing the 
Action of the Papillary Muscles. 



144 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

When valves are so deformed that their orifice is both leaky and 
obstructed, we have what is known as a " combined " or " double " 
valve lesion. 

Since valvular lesions are recognized largely by their results, 
first upon the walls of the heart itself and then upon the other 
organs of the body, it seems best to give some account of these 
results before passing on to the description of the individual le- 
sions in the heart itself. 

The results of valvular lesions are first conservative and later 
destructive. The conservative results are known as : 

The establishment of compensation through hypertrophy. 

The destructive or degenerative results are known as : 

The failure of compensation through (or without) dilatation. 

I shall consider, then, 

(a) The establishment and the failure of compensation. 

(b) Cardiac hypertrophy. 

(c) Cardiac dilatation. 

ESTABLISHMENT AND FAILURE OF COMPENSATION IN 
VALVULAR DISEASE OF THE HEART. 

We may discriminate three periods in the progress of a case of 
valvular heart disease : 

(1) The period before the establishment of compensation. 

(2) The period of compensation. 

(3) The period of failing or ruptured compensation. 

(1) Compensation Not Yet Established. 

In most cases of acute valvular endocarditis, whether of the 
relatively benign or of the malignant type, there is a time when 
the lesion is perfectly recognizable despite the fact that compensa- 
tory hypertrophy has not yet occurred. In some cases this period 
may last for months ; the heart is not enlarged, there is no accentu- 
ation of either second sound at the base, there is no venous stasis, 
and our diagnosis must rest solely upon the presence and character- 
istics of the murmur. For example, in early cases of mitral regur- 



VALVULAR LESIONS. 145 

gitation due to chorea or rheumatism, the disease may be recog- 
nized by the presence of a loud musical murmur heard in the back 
as well as at the apex and in the axilla. In the earlier stages of 
aortic regurgitation occurring in young people as a complication of 
rheumatic fever, there may be absolutely no evidence of the valve 
lesion except the characteristic diastolic murmur. In most text- 
books of physical diagnosis I think too little attention is given to 
this stage of the disease. 

(2) The Period of Compensation. 

Valvular disease would, however, soon prove fatal were it not 
for the occurrence of compensatory hypertrophy of the heart walls. 
To a certain extent the heart contracts as a single muscle, and in- 
creases the size of all its walls in response to the demand for in- 
creased work ; but as a rule the hypertrophy affects especially one 
ventricle — that ventricle, namely, upon which especially demand is 
made for increased power in order to overcome an increased resist- 
ance in the vascular circuit which it supplies with blood. What- 
ever increases the resistance in the lungs brings increased work 
upon the right ventricle ; whatever increases the resistance in the 
aorta or peripheral arteries increases the amount of work which the 
left ventricle must do. 

Now, any disease of the mitral valve, whether obstruction or 
leakage, results in engorgement of the lungs with blood, and hence 
demands an increased amount of work on the part of the right 
ventricle in order to force the blood through the overcrowded pul- 
monary vessels ; hence it is in mitral disease that we find the great- 
est compensatory hypertrophy of the right ventricle. 

On the other hand, it is obvious that obstruction at the aortic 
valves or in the peripheral arteries (arterio-sclerosis) demands an 
increase in power in the left ventricle, in order that the requisite 
amount of blood may be forced through arteries of reduced calibre, 
while if the aortic valve is so diseased that a part of the blood 
thrown into the aorta by the left ventricle returns into that ven- 
tricle, its work is thereby greatly increased, since it has to contract 
upon a larger volume of blood. 
10 



146 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

In response to these demands for increased work, the muscular 
wall of the left ventricle increases in thickness, and compensation is 
thus established at the cost of an increased amount of work on the 
part of the heart. 1 

(3) Failure of Compensation. 

Sooner or later in the vast majority of cases the heart, handi- 
capped as it is by a leakage or obstruction of one or more valves, 
becomes unable to meet the demands made upon it by the needs of 
the circulation. Failure of compensation is sometimes associated 
with dilatation of the heart and weakening of its walls, but in 
many cases no such change can be found to account for its failure, 
and we have to fall back upon changes in the nutrition of the 
heart wall or upon some hypothetical derangement of the ner- 
vous mechanism of the organ as an explanation. Whatever the 
cause may be, the result of ruptured compensation is venous stasis ; 
that is, oedema or dropsy of various organs appears. If the 
left ventricle is especially weakened, dropsy appears first in the 
legs, on account of the influence of gravity, soon after in the geni- 
tals, lungs, liver, and the serous cavities. Engorgement of the 
lungs is especially marked in cases of mitral disease with weakening 
of the right ventricle, and is manifested by dyspnoea, cyanosis, 
cough, and haemoptysis. In many cases, however, dropsy is very 
irregularly and unaccountably distributed, and does not follow the 
rules just given. In pure aortic disease, uncomplicated by leakage 
of the mitral valve, dropsy is a relatively late symptom, and dysp- 
noea and precordial pain (angina pectoris) are more prominent. 

HYPERTROPHY AND DILATATION. 

Since cardiac hypertrophy or dilatation are not in themselves 
diseases, but may occur in any disease of the heart (valvular or 
parietal), it seems best to give some account of them and of the 
methods by which they may be recognized, before taking up sepa- 
rately the different lesions with which they are associated. 

1 Rosenbach brings forward evidence to show that the arteries, the lungs, 
and other organs actively assist in maintaining compensation. 



VALVULAR LESIONS. 147 



1. Cardiac Hypertrophy. 

Hypertrophy of the heart is usually due to the following causes : 

First (and most frequent) : Valvular disease of the heart itself. 
Second: Obstruction of the flow of blood through the arteries 
owing to increase of arterial resistance, such as occurs in chronic 
nephritis and arterio-sclerosis. Third : Obstruction to the circula- 
tion of the blood through the lungs (emphysema, cirrhosis of the 
lung, fibroid phthisis). Fourth: Severe and prolonged muscular 
exertion (athlete's heart). 

In valvular disease the greatest degree of hypertrophy is to be 
seen usually in relatively young persons, and especially when the 
advance of the lesion is not very rapid. 

Hypertrophy of the heart in valvular disease is also influenced 
by the amount of muscular work done by the patient, by the de- 
gree of vascular tension, and by the treatment. In the great major- 
ity of cases of hypertrophy, from whatever cause, both sides of the 
heart are affected, but we may distinguish cases in which one or the 
other ventricle is predominantly affected. 

(1) Cardiac hypertrophy affecting especially the left ventricle. 

(a) The apex impulse is usually lower than normal, often in 
the sixth space, occasionally in the seventh or eighth. 1 It is also 
farther to the left than normal, but far less so than in cases in 
which the hypertrophy affects especially the right ventricle. The 
area of visible pulsation is usually increased, and a considerable por- 
tion of the chest wall may be seen to move with each systole of the 
heart, while frequently there is a systolic retraction of the inter- 
spaces in place of a systolic impulse. 

(b) Palpation confirms the results of inspection and shows us 
also that the apex impulse is unusually powerful. Percussion 
shows in many cases that the cardiac dulness is more intense and 
its area increased downward and to a lesser extent toward the left. 2 

1 This is due partly to a stretching of the aorta, produced by the increased 
weight of the heart. 

2 Post mortem hypertrophy of the left ventricle is often found despite the 
absence of the above signs in life. 



148 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(c) If we listen in the region of the maximum cardiac impulse, 
we generally hear an unusually long and low-pitched first sound, 
which may or may not be of a greater intensity than normal. A 
very loud first sound is much more characteristic of a cardiac neu- 
rosis than of pure hypertrophy of the left ventricle. 

The second sound at the apex (the aortic second sound trans- 
mitted) is usually much louder and sharper than usual. Ausculta- 
tion in the aortic area shows that the second sound at that point is 
loud and ringing in character. Not infrequently the peripheral ar- 
teries (the subclavians, brachials, carotids, radials, and femorals) 
may be seen to pulsate with each systole of the heart. This sign is 
most frequently observed in cases of hypertrophy of the left ven- 
tricle, which are due to aortic regurgitation, but is by no means 
peculiar to this disease and may be repeatedly observed when the 
cardiac hypertrophy is due to nephritis or muscular work. I have 
frequently observed it in athletes, blacksmiths, and others whose 
muscular work is severe. 

The radial pulse wave has no constant characteristics, but de- 
pends rather upon the cause which has produced the hypertrophy 
than upon the hypertrophy itself. 

(2) Cardiac Hypertrophy Affecting Especially the Right Ventricle. 

It is much more difficult to be certain of the existence of en- 
largement of the right ventricle than of the left. Practically we 
have but two reliable physical signs : 

(a) Increase in the transverse diameter of the heart, as shown 
by the position of the apex impulse and by percussion of the right 
and left borders of the heart ; and 

(b) Accentuation of the pulmonic second sound, which is often 
palpable as well as audible. 

The apex beat is displaced both to the left and downward, but 
especially to the left. In cases of long-standing mitral disease, the 
cardiac impulse may be felt in mid-axilla, several inches outside the 
nipple, and yet not lower down than the sixth intercostal space. 
In a small percentage of cases (i.e., when the right auricle is en- 
gorged), an increased area of dulness to the right of the sternum 



VALVULAR LESIONS. 149 

may be demonstrated. Accentuation of the pulmonic second sound 
is almost invariably present in hypertrophy of the right ventricle, 
though it is not peculiar to that condition. It may be heard, for 
example, in cases of pneumonia when no such hypertrophy is pres- 
ent, but in the vast majority of cases of cardiac disease we may 
infer the presence and to some extent the amount of hypertrophy 
of the right ventricle from the presence of a greater or lesser ac- 
centuation of the pulmonic second sound. The radial pulse shows 
nothing characteristic of this type of hypertrophy. 

Epigastric pulsation gives us no evidence of the existence of 
hypertrophy of the right ventricle, despite contrary statements in 
many text-books. Such pulsation is frequently to be seen in per- 
sons with normal hearts, and is frequently absent when the right 
ventricle is obviously hypertrophied. It is perhaps most often due 
to an unusually low position of the whole heart. 

Dilatation op the Heart. 

(1) Acute Dilatation. — Immediately after severe muscular exer- 
tion, as, for example, at the finish of a boat race, or of a two-mile 
run (especially in persons not properly trained), an acute dilatation 
of the heart may occur, and in debilitated or poorly nourished sub- 
jects such an acute dilatation may be serious or even fatal in its 
results. 

(2) Chronic dilatation comes on gradually as a result of valvu- 
lar disease or other cause, and gives rise to practically the same 
physical signs as those of acute dilatation, from which it differs 
chiefly as regards the accompanying physical phenomena and the 
prognosis. Briefly stated, the signs of dilatation of the heart, 
whether acute or chronic, are : 

(a) Feebleness anal irregularity of the apex impulse and of the 
radial impulse, (h) enlargement of the heart, as indicated by inspec- 
tion, palpation, and percussion, and (sometimes) (c) murmurs indi- 
cative of stretching of one or another of the valvular orifices. 



150 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Dilatation of the Left Ventricle. 

Inspection shows little that is not better brought out by palpa- 
tion. Palpation reveals a feeble "flapping" cardiac impulse, or 
a vague shock displaced both downward and to the left and diffused 
over an abnormally large area of the chest wall. Percussion veri- 
fies the position of the cardiac impulse and sometimes shows an 
unusually blunt or rounded outline at the apex of the heart. 

On auscultation, the first sound is usually very short and sharp, 
but not feeble unless it is accompanied by a murmur. In case the 
mitral orifice is so stretched as to render the valve incompetent, or 
in case the muscles of the heart are so fatigued and weakened that 
they do not assist in closing the mitral orifice, a systolic murmur is 
to be heard at the apex of the heart. This murmur is transmitted 
to the axilla and back, but does not usually replace the first sound 
of the heart. The aortic second sound, as heard in the aortic area 
and at the apex, is feeble. 

Dilatation of the right ventricle of the heart is manifested by an 
increase in the area of cardiac dulness to the right of the sternum 
(corresponding to the position of the right auricle), by feebleness of 
the pulmonic second sound together with signs of congestion and 
engorgement of the lungs, and often by a systolic murmur at the 
tricuspid valve; i.e., at or near the. root of the ensiform cartilage. 
When this latter event occurs, one may have also systolic pulsation 
in the jugular veins and in the liver (see below, p. 188). 

In cases of acute dilatation, such as occur in infectious fevers 
or at the end of well-contested races, there is often to be heard a 
systolic murmur loudest in the pulmonary area and due very pos- 
sibly to a dilatation of the conus arteriosus. 

The diagnosis of dilatation of the heart seldom rests entirely 
upon physical signs referable to the heart itself. In acute cases 
our diagnosis is materially aided by a knowledge of the cause, 
which is often tolerably obvious. In chronic cases the best evi- 
dence of dilatation is often that furnished by the venous stasis 
which results from it. 



VALVULAR LESIONS. 151 

(4) CHRONIC VALVULAR DISEASE. 
I. Mitral Regurgitation. 

The commonest and on the whole the least serious of valvular 
lesions is incompetency of the mitral. It results in most cases 
from the shortening, stiffening, and thickening of the valve pro- 
duced by rheumatic endocarditis in early life. It is the lesion 
present in most cases of chorea (see Figs. 86 and 87). 

Temporary and curable mitral regurgitation may result from 
weakening of the heart muscle, which normally assists in closing 
the mitral orifice through the sphincter-like contraction of its cir- 
cular fibres. 

Great muscular fatigue, such as is produced by a hard boat 
race, may result in a temporary relaxation of the mitral sphincter 
or of the papillary muscles sufficient to allow of genuine but tem- 
porary and curable regurgitation through the mitral orifice. In 
conditions of profound nervous debility and exhaustion, similar 
Aveakening of the cardiac muscles may allow of a leakage through 
the mitral, which ceases with the removal of its cause. Stress has 
recently been laid upon these points by Arnold and by Morton 
Prince. 

Mitral insufficiency due to stretching of the ring into which the 
valve is inserted occurs not unfrequently as a result of dilatation 
of the left ventricle, and is commonly known as relative insufficiency 
of the mitral valve. The valve orifice can enlarge, the valve can- 
not, and hence its curtains are insufficient to fill up the dilated ori- 
fice. This type of mitral insufficiency frequently results from 
aortic regurgitation with the dilatation of the left ventricle which 
that lesion produces, or from myocarditis, which weakens the heart 
wall until it dilates and widens the mitral orifice. 

The results of any form of mitral leakage are : 

1. Dilatation or hypertrophy of the left auricle, which has to 
receive blood both from the lungs and through the leaky mitral 
from the left ventricle. 

2. The overfilled left auricle cannot receive the blood from the 



152 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

lungs as readily as it should; hence the blood "backs up " in the 
lungs and thereby increases the work which the right ventricle 
must do in order to force the blood through them. Thus result 
oedema of the lungs, and — 










Fig. 86. 






'-D/jtasa/Jftfta/ 




Fig. 87. 

Fig. 86.— Normal Heart during Systole. Mitral valve closed ; blood flowing through the open 
aortic valves into the aorta. 

Fig. 87.— Mitral Regurgitation. The heart is in systole and the arrows show the current flowing 
back in the left auricle as well as forward into the aorta. 



VALVULAR LESIONS. 153 

(3) Hypertrophy and dilatation of the right ventricle, which in 
turn becomes sooner or later overcrowded so that the tricuspid 
valve gives way and tricuspid leakage occurs. 

(4) The capacity for hypertrophy possessed by the right auricle 
is soon exhausted, and we get then — 

(5) General venous stasis, which shows itself first as venous 
pulsation in the jugulars and in the liver and later in the tissues 
drained by the portal and peripheral veins. This venous stasis in- 
creases the work of the left ventricle, and so we get — 

(6) Hypertrophy and dilatation of the left ventricle. Hyper- 
trophy of the left ventricle is also produced by the increased work 
necessary to maintain some vestige of sphincter action at the leaky 
mitral orifice, as well as by the labor of contracting upon the extra 
quantity of blood delivered to it by the enlarged left auricle. 

At last the circle is complete. Every chamber in the heart is 
enlarged, overworked, and failure is imminent. 

Eeturning now to the signs of mitral regurgitation, we shall find 
it most convenient to consider first the type of regurgitation pro- 
duced by rheumatism and resulting in thickening, stiffening, and 
retraction of the valve. 

Physical Signs. 

(a) First Stage — Prior to the Establishment of Compensation. 

We have but one characteristic physical sign : 

A systolic murmur heard loudest at the apex of the heart, trans- 
mitted to the back (below or inside the left scapula) and to the left 
axilla. The murmur is not infrequently musical in character, and 
when this is the case diagnosis is much easier. Systolic musical 
murmurs so transmitted do not occur without valvular leakage. 
Eosenbach believes that adherent pericardium is capable of produc- 
ing such a murmur, but only, if I understand him rightly, in case 
there is a genuine mitral leakage due to the embarrassing embrace 
of the pericardium which prevents the mitral orifice from closing. 

" Functional " or " hsemic " murmurs are rarely heard in the 
back, and very rarely, if ever, have a musical quality. 



154 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Cases of mitral regurgitation are not very often seen at this 
stage, but in acute endocarditis after the fever and anaemia have 
subsided, or in chorea, such a murmur may exist for days or weeks 
before any accentuation of the pulmonic second sound or any en- 
largement of the heart appears. I have had the opportunity of 
verifying the diagnosis at autopsy in two such cases. 

(b) Second Stage — Compensation Established. 

As long as compensation remains perfect, the only evidence of 
regurgitation may be that obtained by auscultation, and I shall 
accordingly begin with this rather than in the traditional way with 
inspection, palpation, and percussion. 

The distinguishing auscultatory phenomena in cases of well- 
compensated mitral insufficiency are : 

(a) A systolic murmur whose maximum intensity is at or near 
the apex impulse of the heart, but which is also to be heard in the 
left axilla and in the back below or inside the angle of the left 
scapula (so far the signs are those of the first stage, above de- 
scribed). 

(b) A pathological accentuation of the pulmonic second sound. 
This is the minimum of evidence upon which it is justifiable to 

make the diagnosis of compensated mitral regurgitation. In the 
vast majority of cases, however, our diagnosis is confirmed by the 
following additional data: 

(c) Enlargement of the heart as shown by inspection, palpation, 
and percussion. 

(d) Evidence of congestion of the lungs (dyspnoea, orthopncea, 
cough, cyanosis, hemoptysis), as well as of the general venous sys- 
tem (engorgement of the liver, oedema of the legs, ascites, etc.). 

The pulse in well-compensated cases shows no considerable 
abnormality. When compensation begins to fail, or sometimes be- 
fore that time, the most characteristic thing about the pulse is its 
marked irregularity both in force and rhythm. Such irregularity 
is at once more common and less serious in mitral disease than in 
that of any other valve ; it may continue for years and be compat- 
ible with very tolerable health. 



VALVULAR LESLONS. 



155 



Eeturning now to the details of the sketch just given, we will 
take up first— 

(a) The Murmur. — In children the murmur of mitral regurgita- 
tion may be among the loudest of all murmurs to be heard in val- 



lst 



I 



1st 



2nd 



±± 



2nd. 



J_L 



Fig. 88.— Diagram to Represent Systolic Mitral Murmur. The heavy lines represent the normal 
cardiac sounds and the light lines the murmur, which in this case does not replace the first 
sound and k * tapers " off characteristically at the end. . 

vular disease, but this doe's not necessarily imply that the lesion is 
a very severe one. A murmur which grows louder under observar 
tion in a well-compensated valvular lesion may mean an advance of 
the disease, but if the case is first seen after compensation has 
failed a faint, variable whiff in the mitral area may mean the se- 
verest type of lesion. As the patient improves under the influence 
of rest and cardiac tonics, such a murmur may grow very much 
louder, or a murmur previously inaudible may appear. 

The length of the murmur varies a great deal in different cases 
and is not of any great practical importance. It rarely ends 
abruptly, but usually " tails off" at the end of systole (see Fig. 88). 
Musical murmurs are heard more often in mitral regurgitation than 
in any other valve lesion, but the musical quality rarely lasts 
throughout the whole duration of the murmur, contrasting in this 
respect with musical murmurs produced at the aortic valve. The 



2nd 



IIM t 



2nd 



In 1 1 i 1 



Fig. 89.— Systolic Mitral Murmur Replacing the First Sound of the Heart. 



first sound of the heart may or may not be replaced by the murmur 
(see Fig. 89). When the sound persists and is heard either with 
or before the murmur, one can infer that the lesion is relatively 
slight in comparison with cases in which the first sound is wholly 



156 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

obliterated. Post-systolic or late systolic murmurs, which are occa- 
sionally heard in mitral regurgitation, are said to point to a rela- 
tively slight amount of disease in- the valve (see Fig. 90). Eosen- 



lst 



I 



2nd 



1st 



1 



2nd 



Fm. 90.— Late Systolic Murmur. The first sound is clear and an interval intervenes between 

it and the murmur. 

bach claims that the late systolic murmur is always due to organic 
disease of the valves and never occurs as a functional murmur. 

When compensation fails, the murmur may altogether disappear 
for a time, and if the patient is then seen for the first time and 
dies without rallying under treatment, it may be impossible to 




Pulmonic second 
accented. 



Systolic murmur 
loudest here. 



Fig. 91.-Mitral Regurgitation. 



The murmur is heard over the shaded area as well as in the 
back. 



make the diagnosis. The very worst cases, then, are those in which 
there is no murmur at all. 

The murmur of mitral regurgitation is conducted in all directions, 
but especially toward the axilla and to the back {not around the 
chest, but directly). In the latter situation it is usually louder 



VALVULAR LESIONS. 



157 



than it is in mid-axilla, and occasionally it is heard as loudly in the 
back as anywhere else. This is no doubt owing to the position of 
the left auricle (see Figs. 91 and 92). 

(6) After compensation is established and as long as it lasts an 
accentuation of the. pulmonic second sound is almost invariably to 
be made out, and may be so marked that we can feel and see it, as 
well as hear it. Not infrequently one can also see and feel the 
pulsation of the conus arteriosus — not the left auricle — in the second 
and third left intercostal space. (It may be well to mention again 



Systolic murmur. 




Fig. 92.— Mitral Regurgitation. Murmur heard over the shaded area. 



here that by accentuation of the pulmonic second sound one does 
not mean merely that it is louder or sharper in quality than the 
aortic second sound, since this is true in the vast majority of cases 
in healthy individuals under thirty years of age. Pathological ac- 
centuation of the pulmonic second sound means a greater intensity 
of the sound than ive have a right to expect at the age of the individ- 
ual in question.) Occasionally the pulmonic second sound is redu- 
plicated, but as a rule this points to an accompanying stenosis of 
the mitral valve. At the apex the second sound (i.e., the trans- 
mitted aortic second) is not infrequently wanting altogether, owing 



158 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

to the relatively small amount of blood which, recoils upon the 
aortic valves. 

(c) Enlargement of the heart, and more especially of the right 
ventricle, is generally to be made out, and in the majority of cases 
this enlargement is manifested by displacement of the apex impulse 
both downward and toward the left, but. more especially to the 
left. Percussion confirms the results of inspection and palpation 
regarding the position of the cardiac impulse. The normal sub- 
sternal dulness is increased in intensity, and we can sometimes 
demonstrate an enlargement of the heart toward the right (see 
Fig. 91). 

In children (in whom adhesive pericarditis often complicates 
the disease) a systolic thrill may not infrequently be felt at the 
apex, and the precordia may be bulged, and even in adults such a 
systolic thrill is not so rare as some writers would have us sup- 
pose. 

(d) The pulse, as said above, shows nothing characteristic at any 
stage of the disease. While compensation lasts, there is usually 
nothing abnormal about the pulse, although it may be somewhat 
irregular in force and rhythm, and may be weak when compared to 
the powerful beat at the apex in case the regurgitant stream is a 
very large one. Irregularity at this period is less common in pure 
mitral regurgitation than in cases complicated by stenosis. 

(e) Third Stage — Failing Compensation. 

When compensation begins to fail, the pulse becomes weak and 
irregular, and many heart beats fail to reach the wrist, but there 
is still nothing characteristic about the pulse, which differs in no 
respect from that of any case of cardiac weakness of whatever 
nature. 

(e) Evidence of venous stasis, first in the lungs and later in the 
liver, lower extremities, and serous cavities, does not show itself 
so long as compensation is sufficient, but when the heart begins to 
fail the patient begins to complain not only of palpitation and car- 
diac distress, but of dyspnoea, orthopnoea, and cough, and examina- 
tion reveals a greater or lesser degree of cyanosis with pulmo- 



VALVULAR LESIONS. 159 

nary cederaa manifested by crackling rales at the base of the lungs 
posteriorly, and possibly also by hsenioptysis or by evidences of 
hydrothorax (see below, p. 266). If compensation is not re-estab- 
lished, the right ventricle dilates, the tricuspid becomes incompe- 
tent, the liver becomes enlarged and tender, dropsy becomes gen- 
eral, the heart and pulse become more and more rapid and irregular, 
the heart murmur disappears and is replaced by a confusion of 
short valvular sounds, "gallop rhythm" or "delirium cordis" often 
considerably obscured by the noisy, labored breathing with numer- 
ous moist rales. In a patient seen for the first time in such a con- 
dition diagnosis may be impossible, yet mitral disease of some type 
may usually be suspected, since murmurs produced at the aortic 
valve are not so apt to disappear when compensation fails. The 
relative tricuspid insufficiency which often occurs is likely to mani- 
fest itself by an enlargement of the right auricle, sometimes demon- 
strable by percussion and later by venous pulsation in the neck and 
in the liver. 

(d) Differential Diagnosis. 

The murmur of mitral regurgitation may be confused with 

(1) Tricuspid regurgitation. 

(2) Functional murmurs. 

(3) Stenosis or roughening of the aortic valves. 

(1) The post-mortem records of the Massachusetts General 
Hospital show that in the presence of a murmur due to mitral re- 
gurgitation it is very easy to fail altogether to recognize a tricuspid 
regurgitant murmur. Only 5 out of 29 cases of tricuspid regurgi- 
tation found- at autopsy were recognized during life. Allbutt's 
figures from Guy's Hospital are similar. In the majority of these 
cases, mitral regurgitation was the lesion on which attention was 
concentrated during the patient's life. This is all the more excus- 
able because the tricuspid area is so wide and uncertain. Murmurs 
produced at the tricuspid orifice are sometimes heard with maxi- 
mum intensity just inside the apex impulse, and if we have also a 
mitral regurgitant murmur, it may be impossible under such cir- 
cumstances to distinguish it from the tricuspid murmur. Some- 



160 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

times the two are of different pitch, but more often tricuspid regur- 
gitation must be recognized indirectly if at all, i.e., through the 
evidence given by venous pulsation in the jugular veins and in the 
liver. Tricuspid murmurs are not transmitted to the left axilla 
and do not cause accentuation of the pulmonic second sound, al- 
though they are compatible with such accentuation. They are to 
be distinguished from the murmurs of mitral regurgitation by their 
different seat of maximum intensity, possibly by a difference in 
pitch, but most clearly by the concomitant phenomena of venous 
pulsation above mentioned. 

(2) " Functional " murmurs are usually systolic and may have 
their maximum intensity at the apex of the heart, but in the great 
majority of cases they are heard best over the pulmonic valve or 
just inside or outside the apex beat (Potain). They are faint or 
inaudible at the end of expiration, and are more influenced by 
position than organic murmurs are. In the upright position they 
are often very faint. They are rarely transmitted beyond the 
precordia and are unaccompanied by any evidences of enlargement 
of the heart, by any pathological accentuation of the pulmonic 
second sound, 1 or any evidences of engorgement of the lungs or 
general venous system. 

(3) Roughening or narrowing of the aortic valves may produce 
a systolic murmur with maximum intensity in the second right in- 
tercostal space, but this murmur is not infrequently heard all over 
the precordia and quite plainly at the apex, so that it may simulate 
the murmur of mitral regurgitation. The aortic murmur may in- 
deed be heard more plainly at the apex than at any other point ex- 
cept the second right intercostal space, owing to the fact that the 
right ventricle, which occupies most of the precordial region be- 
tween the aortic and mitral areas, does not lend itself well to the 
propagation of certain types of cardiac murmurs. Under these 
circumstances " a loud, rough aortic murmur may be heard at the 

1 It must be remembered that in chlorosis, a disease in which functional 
murmurs are especially prone to occur, the pulmonic second sound is often 
surprisingly loud, owing to a retraction of the left lung, which uncovers the 
root of the pulmonic artery. 



VALVULAR LESIONS. 161 

apex as a smooth murmur of a different tone " (Broaclbent). Such 
a murmur is not, however, likely to be conducted to the axilla or 
heard beneath the left scapula, nor to be accompanied by accentua- 
tion of the pulmonic second sound nor evidences of engorgement 
of the lungs and general venous system. 

II. Mitral Stenosis. 

Narrowing or obstruction of the mitral orifice is almost invari- 
ably the result of a chronic endocarditis which gradually glues to- 
gether the two flaps of the valve until only a funnel-shaped open- 
ing or a slit like a buttonhole is left (see Figs. 93 and 94). As we 
examine post mortem the tiny slit which may be all that is left of 
the mitral orifice in a case of long standing, it is difficult to con- 
ceive how sufficient blood to carry on the needs of the circulation 
could be forced through such an insignificant opening. 

Usually a slow and gradually developed lesion, mitral stenosis 
often represents the later stages of a process which in its earlier 
phases produced pure mitral regurgitation. By some observers the 
advent of stenosis is regarded as representing an attempt at com- 
pensation for a reduction of the previous mitral leakage. Others 
consider that the stenosis simply increases the damage which the 
valve has suffered. 

A remarkable fact never satisfactorily explained is the predilec- 
tion of mitral stenosis for the female sex. A large proportion of 
the cases — seventy-six per cent in my series — occur in women. 

It is also curious that so many cases are associated with pul- 
monary tuberculosis. 

Physical Signs. 

Mitral stenosis may exist for many years without giving rise to 
any physical signs by which it may be recognized, and even after 
signs have begun to show themselves they are more fleeting and 
inconstant than in any other valvular lesion of the heart. In the 
early stages of the disease the heart may appear to be entirely nor- 
mal if the patient is at rest, and especially if examined in the re- 
cumbent position, characteristic signs being elicited only by exer- 
11 



162 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



tion ; or again a murmur which, is easily audible with the patient 
in the upright position may disappear in the recumbent position ; 
or a murmur may be heard at one visit, at the next it may be im- 
possible to elicit it by any manoeuvre, while at the third visit it may 







yte/i. 



? <?/?a*rfJ//&z/. 



Fig. 94. 



Fig. 93.— Diagram to Represent the Position of the Valves in the Normal Heart during Diastole, 
the Open Mitral Allowing the Blood to Flow Down from the Left Auricle, the Aortic Closed. 

Fig. 94.-Mitral Stenosis— Period of Diastole. The blood flowing from the left auricle is ob- 
structed by the thickened and adherent mitral curtains. 



VALVULAR LESIONS. 



163 



be easily heard again. These characteristics ' explain to a certain 
extent the fact that differences of opinion so often arise regarding 
the diagnosis of mitral stenosis, and that out of forty-eight cases in 
which this lesion was found at autopsy at the Massachusetts General 
Hospital, only twenty-three were recognized during life. No com- 
mon lesion (with the exception of tricuspid regurgitation) has been 
so frequently overlooked in our records. 

I shall follow Broadbent in dividing the symptoms into three 
stages, according to the extent to which the lesion has progressed. 

I. 

In the first stage inspection and palpation show that the apex 
beat is little if at all displaced, and percussion reveals no 'mcrease 




Pulmonic second 
accented. 



" Double-shock " 
sound. 



Presystolic murmur 
heard in limited 



Fig. 95. —Mitral Stenosis. 



in the area of cardiac dulness ; indeed, in rare cases the heart may 
be smaller than usual. If one lays the hand lightly over the origin 
of the apex beat, one can generally feel the purring presystolic thrill 
which is so characteristic of this disease, more common indeed than 
in any other. This thrill is more marked in the second stage of 
the disease, but can generally be appreciated even in the first. It 
runs up to and ceases abruptly with the very sharp first sound, 



164 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

the sudden shock of which may be appreciated even by palpation. 
The thrill is sometimes palpable even when no murmur can be 
heard, and often the thrill is transmitted to the axilla when the 
murmur is confined to the apex region. On auscultation one 
hears, especially after the patient has been exerting himself, and 
particularly if he leans forward and to the left, a short rumble or 
roll immediately preceding the systole and increasing in intensity 
as it approaches the first sound (see Fig. 95). At this stage of 
the disease the second sound can still be heard at the apex. The 
first sound is very sharply accented or snapping, and communi- 
cates a very decided shock to the ear when a rigid stethoscope 
is used. As a rule, the murmur is closely confined to the region 
of the apex beat and not transmitted any considerable distance in 
any direction. I have seen cases in which it was to be heard only 



1st 



1st 



2nd ,„i|| 2nd 



1 



Fig. 96.— The Murmur of Mitral Stenosis— First Stage. The place of the murmur and its cres- 
cendo character are indicated by the position of the light lines just before the first sound 
and by their increasing length. 

over an area the size of a half-dollar. 1 Very characteristic of mi- 
tral stenosis is a prolongation of the diastolic pause so that the inter- 
val beween the second sound of one cycle and the first sound of the 
next is unduly long. Occasionally the diastolic sound is redupli- 
cated ("double-shock sound" — Sansom) at this stage of the disease, 
but this is much more frequent in the later phases of the lesion. 2 

Irregularity of the heart beat both in force and rhythm is very 
frequently present even in the early stages of the affection. The 
heart may be regular while the patient is at rest, but slight exer- 
tion is often sufficient to produce marked irregularity. 

1 It may, however, be widely transmitted to the left axilla and audible in 
the back or even over the whole of the left chest, especially when the stenosis 
is combined with regurgitation. • 

2 This is the opinion of most observers. Sansom states that the "double- 
shock sound " may precede all other evidences of mitral stenosis. 



VALVULAR LESIONS. 165 



II. 

In the second stage the murmur and thrill are usually longer and 
may occupy the whole of diastole, beginning with considerable in- 
tensity just after the reduplicated second sound, quickly dimmish - 

lst 




I ml Mill llllllli 



I 



Fig. 97.— Type of Presystolic Murmur Often Heard in the Second Stage of Mitral Stenosis. 
Here the murmur fills the whole of diastole, with a gradual increase of intensity as it ap- 
proaches the first sound. No second sound is audible at the apex. 

ing until it is barely audible, and then again increasing with a 
steady crescendo up to the first sound of the next cycle. 1 These 
changes may be graphically represented as in Figs. 97 and 98. Dia- 
stole is now still more prolonged, so that the characteristic rhythm 
of this lesion is even more marked than in the earlier stages of the 
disease. In many cases at this stage no second sound is to be heard 
at all at the apex, although at the pulmonic orifice it is loud and 
almost invariably double. (This is one of the reasons for believing 
that the second sound which we usually hear at the apex is the 
transmitted aortic second sound. In mitral disease the aortic valves 

1st 



2nd 



ll.„. .111111111111111 1. mill II 



i 



2nd 



Fig. 98.— Type of Presystolic Murmur Sometimes Heard in the Second Stage of Mitral Stenosis. 
There is a double crescendo. Tbe second sound seems reduplicated. 

shut feebly owing to the relatively small amount of blood that is 
thrown into the aorta. ) 

At this stage of the disease enlargement of the heart begins to 
make itself manifest. The apex impulse is displaced to the left — 

1 Rarely one finds a crescendo in the middle of a long presystolic roll with 
a diminuendo as it approaches the first sound. 



166 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

sometimes as far as the mid-axillary line, and often descends to 
the sixth interspace. Occasionally the cardiac dnlness is increased 
to the right of the sternum. 

The instability and fleeting character of the murmur in the ear- 
lier stages of the disease are much less marked in this, the second 
stage. The first sound at the apex still retains its sharp, thump- 
ing quality, and is often audible without the murmur in the back. 

The irregularity of the heart is generally greater at this stage 
than in the earlier one. 

III. 

The third stage of the affection is marked by the disappearance 
of the characteristic murmur, and is generally synchronous with 
the development of tricuspid regurgitation. The right ventricle 
becomes dilated sometimes very markedly. Indeed, it may produce 
a visible pulsating tumor below the left costal border and be mis- 
taken for cardiac aneurism (Osier). The snapping first sound and 
the " double-shock " sound usually remain audible, but the latter 
may be absent altogether. Diagnosis in this stage rests largely upon - 
the peculiar snapping character of the first sound, together with the 
prolongation of diastole and the very great irregularity of the heart, 
both in force and rhythm. At times a presystolic thrill may be 
felt even when no murmur is to be. heard. 

The pulse shows nothing characteristic in many cases except 
that early and persistent irregularity which has been already al- 
luded to. In other cases the wave is low, long, easily compressed, 
but quite perceptible between beats ; but for the lack of sufficient 
power in the cardiac contractions the pulse would be one of high 
tension. 

As the disease advances the irregularity of the pulse becomes 
more and more marked, and sometimes presents an amazing contrast 
with the relatively good general condition of the circulation. Even 
when not more than a third of the beats reach the wrist, the patient 
may be able to attend to light work and feel very well. Such cases 
make us feel as if a pulse were a luxury rather than a necessity. 

Under the influence of digitalis the pulse is especially apt to 



VALVULAR LESIONS. 167 

assume the bigeminal type in mitral stenosis. Every other beat is 
then so abortive that it fails to send, a wave to the wrist, and the 
weak beat is succeeded by a pause. According to Broadbent the 
weak beat corresponds to an abortive contraction of the left ven- 
tricle accompanied by a normal contraction of the right ventricle, 
so that for each two strong beats of the right side of the heart we 
have one strong and one weak beat of the left side of the heart. 

Mitral stenosis is in the great majority of cases combined with 
mitral regurgitation, and it often happens that the signs of regur- 
gitation are so much more prominent than those of stenosis that 
the latter escape observation altogether, especially in the third 
stage of the disease, when the typical presystolic roll has disap- 
peared. In such cases combined stenosis and regurgitation is to be 
distinguished from pure regurgitation by the sharpness of the first 
sound, which would be very unusual at this stage of a case of pure 
mitral regurgitation. The presence of reduplicated second sound, a 
" double-shock sound " at the outset of the prolonged diastolic pause, 
and of great irregularity in force and rhythm, is further suggestive 
of mitral stenosis. 

Mitral stenosis is apt to be associated with haemoptysis, with en- 
gorgement of the liver and ascites, and especially with arterial em- 
bolism. No other valve lesion is so frequently found associated 
with embolism. The lungs are generally very voluminous, and 
may therefore mask an increase in area or intensity of the cardiac 
dulness. 

Differential Diagnosis. 

I have already discussed the difficulty of distinguishing a double 
lesion at the mitral valve from a simple mitral regurgitation (see 
above, p. 161). 

Other murmurs which may be mistaken for the murmur of mi- 
tral stenosis are : 

(a) The Austin Mint murmur. 

(b) The murmur of tricuspid stenosis. 

(c) A rumbling murmur sometimes heard in children, after an 
attack of pericarditis. 



168 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(a) The Austin Flint niurnmr. 

In 1862 Austin Flint studied two cases in which during life a 
typical pre systolic roll was audible at the apex of the heart, yet in 
which post mortem the mitral valve proved to be perfectly normal, 
and the only lesion present was aortic insufficiency. This observation 
has since been verified by Osier, Brain well, Gairdner, and other com- 
petent observers. At the Massachusetts General Hospital we have 
had seven such cases with autopsy. Yet, despite repeated confir- 
mation, Flint's observation has remained for nearly forty years un- 
known to physicians at large. Its importance is this : Given a case 
of aortic regurgitation — a presystolic murmur at the apex does not 
necessarily mean stenosis of the mitral valve even though the mur- 
mur has the typical rolling quality and is accompanied by a pal- 
pable thrill. It may be only one of the by-effects of the aortic 
incompetency. How it is that a presystolic murmur can be pro- 
duced at the apex in cases of aortic regurgitation has been much 
debated. Some believe it is due to the impact of the aortic regur- 
gitant stream upon the ventricular side of the mitral valve, floating 
it out from the wall of the ventricle so as to bring it into contact 
with the stream of blood descending from the left auricle. Others 
suppose that the mhigling of the two currents of blood, that from 
the mitral and that from the aortic orifice, is sufficient to produce 
the murmur. 

Between the " Austin Flint murmur " thus defined and the mur- 
mur of true mitral stenosis, complicating aortic regurgitation, diag- 
nosis may be impossible. If there are no dilatation of the mitral 
orifice and no regurgitation, either from this cause or from deformi- 
ties of the mitral valve itself, any evidence of engorgement of the 
pulmonary circuit (accentuation of the pulmonic second sound, 
oedema of the lungs, haemoptysis, and cough) speaks in favor of an 
actual narrowing of the mitral valve, while the absence of such 
signs and the presence of a predominating hypertrophy of the left 
ventricle tend to convince us that the murmur is of the type de- 
scribed by Austin Flint, i.e., that it does not point to any sten- 
osis of the mitral valve. The sharp, snapping first sound and 
systolic shock so characteristic of mitral stenosis are said to be 



VALVULAR LESIONS 169 

modified or absent in connection with murmurs of the Austin Flint 
type. 

(b) Tricuspid obstruction. 

Luckily for us as diagnosticians, stenosis of the tricuspid valve 
is a very rare lesion. Like mitral stenosis it is manifested by a 
presystolic roiling murmur whose point of maximum intensity is 
sometimes over the traditional tricuspid area, but may be at a point 
so near the mitral area as to be easily confused with stenosis of 
the latter valve. 

The difficulty of distinguishing tricuspid stenosis from mitral 
stenosis is further increased by the fact that the two lesions almost 
invariably occur in conjunction. Hence we have two presystolic 
murmurs, perhaps with slightly different points of maximum inten- 
sity and possibly with a difference in quality, but often quite un- 
distinguishable from each other. In the vast majority of cases, 
therefore, tricuspid stenosis is first recognized at the autopsy, and 
the diagnosis is at best a very difficult one. 

(c) Broadbent, Eosenbach, and others have noticed in children 
who have just passed through an attack of pericarditis a rumbling 
murmur near the apex of the heart, which suggests the murmur of 
mitral stenosis. It is distinguished from the latter, however, by the 
absence of any accentuation of the first sound at the apex, as well 
as by the conditions of its occurrence and by its transiency. Such 
cases are important, since their prognosis is much more favorable 
than that of mitral stenosis. 

Phear (Lancet, September 21, 1895) investigated 46 cases in 
which a presystolic murmur was observed during life and no mitral 
lesion found at autopsy. In 17 of these there was aortic regurgi- 
tation at autopsy ; in 20 of these there was adherent pericardium 
at autopsy ; in 9 nothing more than dilatation of the left ventricle 
was found. In none of these cases was the snapping first sound, 
so common in mitral stenosis, recorded during life. 

It should be remembered that patients suffering from mitral 
stenosis are very frequently unaware of any cardiac trouble, and 
seek advice for anaemia, wasting, debility, gastric or pulmonary 
complaints. This is less often true in other forms of valvular dis- 



170 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

ease. We should be especially on our guard in cases of supposed 
"nervous arrhythmia" or "tobacco heart/' if there has been an at- 
tack of rheumatism or chorea previously. Such cases may present 
no signs of disease except the irregularity — yet may turn out to 
be mitral stenosis. 

IV. Aortic Kegurgitatiox. 

Eheumatic endocarditis usually occurs in early life and most 
often attacks the mitral valve. The commonest cause of aortic dis- 
ease on the other hand — arterio-sclerosis — is a disease of late mid- 




\/tft&a/ (f/t/i/. 



Fig. 99.— Diastole in Aortic Regurgitation. The blood is flowing back through the stumpy and 
incompetent aortic valves. 

die life, and attacks men much more often than women. When 
we think of aortic regurgitation, the picture that rises before us is 
usually that of a man past middle life and most often from the 
classes who live by manual labor. Nevertheless cases occur at all 
ages and in both sexes, and rheumatic endocarditis does not spare 
the aortic cusps altogether by any means. 

Whether produced by arterio-sclerosis extending down from the 
aorta, or by rheumatic or septic endocarditis, the lesion which re- 
sults in aortic regurgitation is usually a thickening and shortening 
of the cusps (see Fig. 99). In rare cases an aortic cusp may be 
ruptured as a result of violent muscular effort, and the signs and 



VALVULAR LESIONS. 171 

symptoms of regurgitation then appear suddenly. But as a rule 
the lesion comes on slowly and insidiously, and unless discovered 
accidentally or in the course of routine physical examination it may 
exist unnoticed for years. Dropsy and cyanosis are relatively late 
and rare, and the symptoms which first appear are usually those of 
dyspnoea and precordial distress. 

It is a disputed point whether relative and temporary aortic 
insufficiency due to stretching of the aortic orifice ever occurs. If 
it does occur, it is certainly exceedingly rare, as the aortic ring is 
very tough and inelastic. 

Dilatation of the aortic arch — practically diffuse aneurism — oc- 
curs in almost every case of aortic regurgitation, and produces sev- 
eral important physical signs. This complication is a very well- 
known one, but has not, I think, been sufficiently insisted on in 
text-books of physical diagnosis. It forms part of that general 
enlargement of the arterial tree which is so characteristic of the 
disease. 

Physical Signs. 

Inspection reveals more that is important in this disease than 
in any other valvular lesion. In extreme cases the patient's face 
or hand may blush visibly with every systole. Not infrequently 
one can make the diagnosis across the room or in -the street by not- 
ing the violent throbbing of the carotids, which may be such as to 
shake the person's whole head and trunk, and even the bed on 
which he lies. ISTo other lesion is so apt to cause a heaving of the 
whole chest and a bobbing of the head, and no other lesion so often 
causes a bulging of the precordia, for in no other lesion is the en- 
largement of the heart so great (cor bovinum or ox-heart) . The 
throbbing of the dilated aorta can often be felt and sometimes seen 
in the suprasternal notch or in the second right interspace. Not 
only the carotids but the subclavians, the brachials and radials, 
the femoral and anterior tibial, and even the digital and dorsalis 
pedis arteries may visibly pulsate, and the characteristic jerking 
quality of the pulse may be seen as well as felt. This visible pul- 
sation in the peripheral arteries, while very characteristic of aortic 



172 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

regurgitation, is occasionally seen in cases of simple hypertrophy of 
the heart from hard muscular work (e.g., in athletes). If the ar- 
teries are extensively calcified, their pulsation become much less 
marked. 

The peculiar conditions of the circulation whereby it is "changed 
into a series of discontinuous discharges as if from a catapult" (All- 
butt) throws a great tensile strain upon all the arteries, and results, 
in almost every long-standing case, in increasing both their length 



Pulsation at the jugulum. 
/ 



Dulness and pul- 
sation cor re- ~-" 
sponding to the 
dilated aortic 
arch. 




Pulsating car- 
otids. 



Diastolic murmur. 



Displaced cardiac 
impulse. 



Fig. 



100.— Aortic Regurgitation, Showing Position of the Diastolic Murmur and Areas of Visible 

Pulsation. 



and their diameter. The visible arterial trunks become tortuous 
and distended, while the arch of the aorta is diffusely dilated and 
becomes practically an aneurism (see Fig. 100). With each heart 
beat the snaky arteries are often jerked to one side as well as made 
to throb. 

Inspection of the region of the cardiac impulse almost always 
shows a very marked displacement of the apex beat both downward 
and outward (but especially the former), corresponding to the hy- 
pertrophy of the left ventricle, which is usually very great, and to 



VALVULAR LESIONS. 173 

the downward sagging of the enlarged aorta. In a small propor- 
tion of the cases no enlargement of the heart is to be demonstrated. 
This was trae of 5 out of the last 67 cases which I have notes of, 
and generally denotes an early and slight lesion. Not at all infre- 
quently one finds a systolic retraction of the interspaces near the 
apex beat instead of a systolic impulse. This is probably due to 
the negative pressure produced within the chest by the powerful 
contraction of an hypertrophied heart. In the suprasternal notch 
one often feels as well as sees a marked systolic pulsation trans- 
mitted from the arch of the dilated aorta, and sometimes mistaken 
for saccular aneurism. 

Arterial pulsation of the liver and spleen are rarely demon- 
strable by a combination of sight and touch. 

Capillar?/ Pulsation. 

If one passes the end of a pencil or other hard substance once 
or twice across the patient's forehead, and then watches the red 
mark so produced, one can often see a systolic flushing of the hyper- 
semic area with each beat of the heart. This is by far the best 
method of eliciting this phenomenon. It may also be seen if a glass 
slide is pressed against the mucous membrane of the lip so as par- 
tially to blanch it, or if one presses upon the finger-nail so as par- 
tially to drive the blood from under it ; but in both these manoeuvres 
error may result from inequality in the pressure made by the ob- 
server upon the glass slide or upon the nail. Very slight movements 
of the observer's fingers, even such as are caused by his own pulse, 
may give rise to changes simulating capillary pulsation. Capillary 
pulsation of normal tissues is not often seen in any condition other 
than aortic 1 regurgitation, yet occasionally one meets with it in 
diseases which produce very low tension of the pulse, such as 
phthisis or typhoid, anaemic and neurasthenic conditions, and I 
have twice seen it in perfectly healthy persons. In such cases the 
pulsation is usually less marked than in aortic regurgitation. 
Rarely pulsation may be detected in the peripheral veins. 

1 Jumping toothache and throbbing felon are common examples of capil- 
lary pulsation in inflamed areas. 



174 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Palpation. 

Palpation verifies the position of the cardiac impulse and the 
heaving of the whole chest wall suggested by inspection. The 
shock of the heart is very powerful and deliberate unless dilatation 






Fig. 101.— Sphygmographic Tracing from Normal Pulse. 

is extreme, when it becomes wavy and diffuse. In the supraclavic- 
ular notch a systolic thrill is often to be felt. A diastolic thrill 
in the precordia is very rare. 

The pulse is important, usually characteristic. The wave rises 



Fig. 103.— Sphygmographic Tracing of the "Pulsus CeUr" in Aortic Regurgitation. Its col- 
lapsing character is well shown. 

very suddenly and to an unusual height, then collapses completely 
and with great rapidity (pulsus celer) (see Figs. 101, 102). 

This type of pulse, which is known as the "Corrigan pulse " or 
"water-hammer pulse," is exaggerated if one raises the patient's 
arm above the head so as to make the force of gravity aid in emp- 
tying the artery. The quality of the pulse in aortic regurgitation 



VALVULAR LESIONS. 175 

is due to the fact that a large volume of blood is suddenly and for- 
cibly thrown into the aorta by the hypertrophied and dilated left 
ventricle, thus causing the characteristically sharp and sudden rise 
in the peripheral arteries. The arteries then empty themselves in 
two directions at once, forward into the capillaries and backward 
into the heart through the incompetent aortic valves; hence the 
sudden collapse in the pulse which, together with its sharp and 
sudden rise, are its important characteristics. The arteries are 
large and often elongated so as to be thrown into curves. 

Kot infrequently one can demonstrate that the radial pulse is 
delayed or follows the apex impulse after a longer interval than 
in normal persons. While compensation lasts, the pulse is usually 
regular in force and rhythm. Irregularity is therefore an especially 
grave sign, much more so than in any other valvular lesion. 

Percussion. 

Percussion adds but little to the information obtained by inspec- 
tion and palpation, but verifies the results of these methods of in- 
vestigation respecting the increased size of the heart, and especially 
of the left ventricle, which may reach enormous dimensions, espe- 
cially in cases occurring in young persons. The heart may be 
increased to more than four times its normal weight. 

Auscultation. 

In rare cases there may be absolutely no murmur and the diag- 
nosis may be impossible during life, though it may be suspected 
by reason of the above-mentioned signs in the peripheral arteries. 
But although the murmur is seldom entirely absent, it is often so 
faint as to be easily overlooked. This is especially true in cases 
occurring in elderly people, and when the patient has been for a 
considerable time at rest. The difficulty of recognizing certain 
cases of aortic regurgitation during life is shown by the fact that 
out of sixty -five cases of aortic regurgitation demonstrated at au- 
topsy in the Massachusetts General Hospital, only forty-four were 
recognized during life. 



176 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

In the majority of cases, however, the characteristic diastolic 
murmur is easily heard if one listens in the right place, and when 
heard it is the most distinctive and trustivorthy of all cardiac mur- 
murs. It almost invariably points to aortic regurgitation and to 
nothing else. 

The murmur of aortic regurgitation, as has been already men- 
tioned, is diastolic in time. 1 Its maximum intensity is usually not 




Fig. 103.— Position of the Point of Maximum Intensity of the Murmur of Aortic Regurgitation. 
The dots are most thickly congregated where the murmur is oftenest heard. 



in the conventional aortic area (second right interspace), but on the 
left side of the sternum about the level of the fourth left costal carti- 
lage. In about one-tenth of the cases, and especially when the 
aortic arch is much dilated, the murmur is best heard in the con- 
ventional aortic area. Occasionally there are two points at which 
it may be loudly heard — one in the second right interspace and the 
other at or near the apex of the heart, while between these points 

1 Another murmur, systolic in time, which almost always accompanies 
the diastolic murmur, is usually due to roughening of the edges of the aortic 
valves or to dilatation of the aortic arch. This murmur must not be assumed 
to mean aortic stenosis (see below, p. 184 J). 



VALVULAR LESIONS. 177 

the murmur is faint. This is probably due to the fact that the 
left ventricle, through which the murmur is conducted, approaches 
the surface of the chest only at the apex, while the intermediate space 
is occupied by the right ventricle, which often fails readily to trans- 
mit murmurs produced at the aortic orifice. Less frequently the 
murmur of aortic regurgitation is heard with maximum intensity 
at the second or third left costal cartilage or in the region of the 
ensiform cartilage (see Fig. 103). 

From its seat of maximum intensity (i.e., usually from the 
fourth left costal cartilage) the murmur is transmitted in all direc- 
tions, but not often beyond the precordia. In about one-third of 
the cases it is transmitted to the left axilla or even to the back. 
It is sometimes to be heard in the subclavian artery and the 
great vessels of the neck; in other cases two heart sounds are 



1st 



2nd 



1st 

2nd 



1 



Fig. 104.— Short Diastolic Murmur Not Replacing the Second Sound. 

audible in the carotid, but no murmur. The murmur is usually 
blowing and relatively high pitched, sometimes musical. Its inten- 
sity varies much, but is most marked at the beginning of the mur- 
mur, giving the impression of an accent there. It may occupy the 
whole of diastole or only a small portion of it — usually the earlier 
portion (see Fig. 104). Late diastolic murmurs are rare. The mur- 
mur may or may not replace the second sound of the heart. Broad- 
bent believes that when it does not obliterate the second sound, 
the lesion is usually less severe than when only the murmur is to 
be heard. Allbutt dissents from this opinion. 

In listening for the aortic second sound with a view to gauging 
the severity of the lesion, it is best to apply the stethoscope over the 
right carotid artery, as here we are less apt to be confused by the 
murmur or by the pulmonic second sound. 

The position of the patient's body has but little effect upon the 
murmur — less than upon murmurs produced at the mitral orifice. 
12 



178 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

The first sound at the apex is generally loud and long. There 
is no accentuation of the pulmonic second. 

Over the larger peripheral arteries, especially over the femoral 
artery, one hears in most cases a sharp, short systolic sound ("pis- 
tol-shot sound ") due to the sudden filling of the unusually empty 
artery ; this sound is merely an exaggeration of what may be heard 
in health. Pressure with the stethoscope will usually bring out a 
systolic murmur (as also in health), and occasionally a diastolic 
murmur as well (Duroziez's sign). This diastolic murmur in the 
peripheral arteries, obtained on pressure with the stethoscope, is 
practically never heard except in aortic regurgitation. It is thought 
by some to be due. to the regurgitant current in the great vessels 
which in very marked cases may extend as far as the femoral ar- 
tery. Duroziez's sign is a comparatively rare one, not present in 
most cases of aortic regurgitation, and usually disappears when 
compensation fails. 

Summary and Differential Diagnosis. 

A diastolic murmur heard with the maximum intensity about 
the fourth left costal cartilage (less often in the second right inter- 
space or at the apex) gives us almost complete assurance of the 
existence of aortic regurgitation. From pulmonary regurgitation, 
an exceedingly rare lesion, the disease is distinguished by the pres- 
ence of predominating hypertrophy of the left ventricle with a 
heaving apex impulse and by the following arterial phenomena : 

(a) Visible pulsation in the peripheral arteries. 

(b) Capillary pulsation. 

(c) " Corrigan " pulse. 

(d) " Pistol-shot sound " in the femoral artery. 

(e) Duroziez's sign. 

The very rare functional diastolic murmur, transmitted from 
the veins of the neck and heard over the base of the heart in cases 
of grave ansernia, may be obliterated by pressure over the bulbus 
jugularis. Such pressure has no effect upon the murmur of aortic 
regurgitation. 

It must be remembered that aortic regurgitant murmurs are 



VALVULAR LESIONS. 179 

often exceedingly faint, and should be listened for with the greatest 
care and under the most favorable conditions. 

Estimation of the Extent and Gravity of the Lesion* 

The extent of the lesion is roughly proportional to — 

(a) The amount of hypertrophy of the left ventricle. 

(b) The degree to which the pulse collapses during diastole 
(provided the radial is not so much calcified as to make collapse 
impossible) . 

(c) The degree to which the murmur replaces the second sound 
as heard over the right carotid artery (Broadbent). 

Irregularity of the pulse is a far more serious sign in this dis- 
ease than in lesions of the mitral valve, and indicates the beginning 
of a serious failure of compensation. 

Another grave sign is a diminution in the intensity of the 
murmur. 

Complications. 

(1) Dilatation of the Aorta. — Diffuse dilatation of the aortic arch 
is usually associated with aortic regurgitation and may produce a 
characteristic area of dulness to the right of the sternum (see Fig. 
100). Not infrequently this dilatation is the cause of a systolic 
murmur to be heard over the region of the aortic arch and in the 
great vessels of the neck. 

(2) Roughening of the Aortic Valves. — In the great majority of 
cases of aortic regurgitation the valves are sufficiently roughened 
to produce a systolic murmur as the blood flows over them. This 
murmur is heard at or near the conventional aortic area, and may 
be transmitted into the carotids. (The relation of these murmurs 
to the diagnosis of aortic stenosis will be considered with the latter 
lesion.) 

(3) The return of arterial blood through the aortic valves into 
the left ventricle produces in time both hypertrophy and dilatation 
of this chamber, and results ultimately in a stretching of the mitral 
orifice which renders the mitral curtains imcompetent. The result 
is a " relative mitral insufficiency " i.e., one in which the mitral valve 



180 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

is intact but too short to reach across the orifice which it is in- 
tended to close. Such an insufficiency of the mitral occurs in most 
well-marked cases ; it temporarily relieves the overdistention of the 
left ventricle and often the accompanying angina, although at the 
cost of engorging the lungs. 1 

(4) The Austin Flint Murmur. — The majority of cases of aortic 
regurgitation are accompanied by a presystolic murmur at the apex, 
which may be due to a genuine mitral stenosis or may be produced 
in the manner suggested by Austin Flint. (For a fuller discussion 
of this murmur see above, p. 168.) 

(5) Aortic stenosis frequently supervenes in cases of aortic re- 
gurgitation, and results in a more or less temporary improvement in 
the patient's condition. It has the effect of increasing the intensity 
of the diastolic murmur, since the regurgitating stream has to pass 
through a smaller opening. 

The general visible arterial pulsation becomes much less marked 
if stenosis supervenes on regurgitation. 



AORTIC STENOSIS. 

Uncomplicated aortic stenosis is by far the rarest of the valvu- 
lar lesions of the left side of the heart, as well as the most difficult 
to recognize. Out of two hundred and fifty-two autopsies made at 
the Massachusetts General Hospital in cases of valvular disease 
there was not one of uncomplicated aortic stenosis. Twenty-nine 
cases occurred in combination with aortic regurgitation. During 
life the diagnosis of aortic stenosis is frequently made, but often on 
insufficient evidence — i.e., upon the evidence of a systolic murmur 
heard with maximum intensity in the second right intercostal space 
and transmitted into the vessels of the neck. Such a murmur does 
indeed occur in aortic stenosis, but is by no means peculiar to this 
condition. Of the other diseases which produce a similar murmur 
more will be said under Differential Diagnosis. 

1 This relative insufficiency of the mitral valve has been termed its "safety- 
valve" action, but the safety is but temporary and dearly bought. 



VALVULAR LESIONS. 



181 



For the diagnosis of aortic stenosis we need the following evi- 
dence : 

(1) A systolic murmur heard best in the second right intercostal 
space and transmitted to the neck. 

(2) The characteristic pulse (vide infra). 

(3) A palpable thrill (usually). 

(4) Absence or great enfeeblement of the aortic second sound. 
Of these signs the characteristic pulse is probably the most im- 




Fig. 105.— Aortic Stenosis. The heart is in systole and the blood column is obstructed by the 
narrowed aortic ring. The mitral is closed (as it should be). 

portant, and no diagnosis of aortic stenosis is possible without it. 
The heart may or may not be enlarged. 

Each of these points will now be described more in detail. 



(1) The Murmur. 

(a) The maximum intensity of the murmur, as has already been 
said, is usually in the second right intercostal space near the ster- 
num or a little above that point near the sterno-clavicular articula- 
tion, but it is by no means uncommon to find it lower down, i.e., 
in the third, fourth, or fifth right interspace, and occasionally it is 
best heard to the left of the sternum in the second or third inter- 
costal space, (b) The time of the murmur is late si/stolie; that is, 



182 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

it follows the apex impulse at an appreciable interval, contrasting 
in this respect with the systolic murmur usually to be heard in 
mitral regurgitation, (c) The murmur is usually widely transmit- 
ted, often being audible over the whole chest and occasionally over 
the skull and the arterial trunks of the extremities (see Fig. 106). 
It is usually heard less well over that portion of the precordia oc- 
cupied by the right ventricle, while, on the other hand, it is rela- 
tively loud hi the region of the apex impulse, whither it is trans- 
mitted through the left ventricle. The same line of transmission 



Maximum intensity 
of systolic mur- 
mur and thrill. 




Fig. 106.— Aortic Stenosis. 



The murmur is audible over the shaded area and sometimes over 
the whole chest. 



was mentioned above as characteristic of the murmur of aortic re- 
gurgitation in many cases. The murmur is also to be heard over 
the carotids and subclavians, and can often be traced over the tho- 
racic aorta along the spine and down the arms. 

Until compensation fails the murmur is apt to be a very loud 
one, especially in the recumbent position; it is occasionally au- 
dible at some distance from the chest, and is often rough and 
vibrating, sometimes musical or croaking. Its length is unusually 
great, extending throughout the whole of systole, but to this rule 
there are occasional exceptions. The first sound in the aortic re- 



VALVULAR LESIONS. 183 

gion is altogether obliterated, as a rule, and the second sound is 
either absent or very feeble. 1 

(2) The Pulse. 

Owing to the opposition encountered by the left ventricle in 
its attempt to force blood into the aorta, its contraction is apt to 
be prolonged ; hence the pulse wave rises gradually and late, and falls 
away slowly. This is shown very well in sphygmographic tracings 
(see Fig. 107) . But further, the blood thrown into the aorta by the 
left ventricle is prevented, by the narrowing of the aortic valves, 
from striking upon and expanding the arteries with its ordinary 
force ; hence the pulse wave is not only slow to rise but small in 




Fig. 107.— Sphygmographic Tracing of the Pulse in Uncomplicated Aortic Stenosis. Compare 
with the normal pulse wave and with that of aortic regurgitation (page 174). 

height, contrasting strongly with the powerful apex beat ("pulsus 
parvus"). Again, the delay in the emptying of the left ventricle, 
brought about by the obstruction at the aortic valves, renders the 
contractions of the heart relatively infrequent, and hence the pulse 
is infrequent (pulsus varus) as well as small and slow to rise. The 
"pjulsus rarus, parvus, tardus " is, therefore, a most constant and 
important point in diagnosis, but unfortunately it is to be felt 
in perfection only in the very rare cases in which aortic stenosis 
occurs uncomplicated. When stenosis is combined with regurgita- 
tion, as is almost always the case, the above -de scribed qualities of 
the pulse are greatly modified as a result of the regurgitation. It 
is also to be remembered that the pulse of aortic stenosis is by no 

1 "Occasionally, as noted by W. H. Dickinson, there is a musical murmur 
of great intensity in the region of the apex, probably due to a slight regurgita- 
tion at high pressure through the mitral valve."— Osler. 



184 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

means unalterable and does not exhibit its typical plateau at all 
times. 

A less characteristic, but decidedly frequent, variation in the 
pulse wave of aortic stenosis is the anacrotic curve. The slow, 
long pulse with a long plateau at the summit is seen also in some 
cases of mitral stenosis and renal disease, and is not peculiar to 
aortic stenosis, but taken in connection with the other signs of the 
disease it has great value in diagnosis. 

(3) The Thrill. 

In the majority of cases an intense purring vibration may be 
felt if the hand is laid over the upper portion of the sternum, espe- 
cially over the second right intercostal space. This thrill is con- 
tinued into the carotids, can occasionally be felt at the apex, and 
rarely over a considerable area of the chest. It is a very important 
aid in the diagnosis of aortic stenosis, but is by no means pathog- 
nomonic, since aneurism may produce a precisely similar vibration 
of the chest wall. 

The heart is slightly enlarged to the left and downward as a 
rule, but the apex impulse is unusually indistinct, " a well-defined 
and deliberate push of no great violence" (Broadbent). Corre- 
sponding to the protracted sustained systole the first sound at the 
apex is dull and long, but not very loud. 

Differential Diagnosis. 

A systolic murmur heard loudest in the second right intercostal 
space is by no means peculiar to aortic stenosis, but may be due to 
any of the following conditions : 

(a) Koughening, stiffness, fenestration, or slight congenital mal- 
formation of the aortic valves. 

(b) Koughening or diffuse dilatation of the arch of the aorta. 

(c) Aneurism of the aorta or innominate artery. 

(d) Functional murmurs. 

(e) Pulmonary stenosis. 
(/) Open ductus arteriosus. 
(g) Mitral regurgitation. 



VALVULAR LESIONS. 185 

(a and b) The great majority of such systolic murmurs at the 
base of the heart, first appearing after middle life, are due to the 
causes mentioned above under a, b, and c. In such cases it is usu- 
ally combined with accentuation and ringing quality of the aortic 
second sound owing to the arterio -sclerosis and high arterial tension 
associated with the changes which produce the murmur. This 
accentuation of the aortic second sound enables us, except in extraor- 
dinarily rare cases, to exclude aortic stenosis, in which the intensity 
of the aortic second sound is almost always much reduced. 

Diffuse dilatation of the aorta, such as often accompanies aortic 
regurgitation, is a frequent cause of a systolic murmur loudest in 
the second right interspace. This may be recognized in certain 
cases by the characteristic area of dulness on percussion and by its 
association with aortic regurgitation of long standing (see Fig. 100) . 

Roughening of the intima of the aorta (endaortitis) is always to 
be suspected in elderly patients with calcified and tortuous periph- 
eral arteries, and such a condition of the aorta doubtless favors the 
occurrence of a murmur, especially when accompanied by a slight 
degree of dilatation. The absence of a thrill and a long, slow 
pulse with a low maximum serves to distinguish such murmurs 
from those of aortic stenosis. 

(c) Aneurism of the ascending arch of the aorta or of the in- 
nominate artery may give rise to every sign of aortic stenosis except 
the characteristic pulse and the diminution of the aortic second 
sound. In aneurism we may have a well-marked tactile thrill and 
a loud systolic murmur transmitted into the neck, but there is 
usually some pulsation to be felt in the second right intercostal 
space and often some difference in the pulses or in the pupils, as 
well as a history of pain and symptoms of pressure upon the tra- 
chea and bronchi or recurrent laryngeal nerve. In aneurism the 
aortic second sound is usually loud and accompanied by a shock, 
and the pulse shows none of the characteristics of aortic stenosis. 

(d) Functional murmurs, sometimes known as "hsemic," are 
occasionally best heard in the aortic area instead of in their usual 
situation (second left intercostal space). They occur especially in 
young, anaemic persons, are not accompanied by any cardiac en- 



186 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

largeraent, by any palpable thrill, any diminution in the aortic 
second sound, or any distinctive abnormalities in the pulse. 

(e) Pulmonary stenosis, an exceedingly rare lesion, is mani- 
fested by a systolic murmur and by a thrill whose maximum inten- 
sity is usually on the left side of the sternum. In the rare cases 
in which this murmur is best heard in the aortic area it may be 
distinguished from the murmur of aortic stenosis by the fact that 
it is not transmitted into the vessels of the neck, has no effect upon 
the aortic second sound, and is not accompanied by the character- 
istic changes in the pulse. 

(/) The murmur due to persistence of the ductus arteriosus 
may last through systole and into diastole ; it may be accompanied 
by a thrill, but does not affect the aortic second sound nor the 
pulse. 

(g) The systolic murmur of aortic stenosis may be heard loudly at 
the apex, and hence the lesion may be mistaken for mitral regur- 
gitation. But the maximum intensity of the murmur of aortic 
stenosis is almost invariably in the aortic area, and its association 
with a thrill and a long, slow pulse should enable us easily to dif- 
ferentiate the two lesions. 

By the foregoing differentiae aortic stenosis may be distinguished 
from the other conditions which resemble it, provided it occurs 
uncomplicated, but unfortunately this is very rare. As a rule, it 
occurs in connection with aortic regurgitation, and its characteristic 
signs are therefore obscured or greatly modified by the signs of the 
latter disease. We may suspect it in such cases (provided the mi- 
tral valve is sufficient) when we have, in addition to the signs of 
aortic regurgitation, a systolic murmur and palpable thrill in the 
aortic area transmitted into the great vessels, a modification of the 
Corrigan pulse in the direction of the "pulsus tardus, varus, par- 
vus," and less visible arterial pulsation than is to be expected in 
pure aortic regurgitation. 

Occasionally one can watch the development of an aortic steno- 
sis out of what was formerly a pure regurgitant lesion, the stenosis 
gradually modifying the characteristics of the previous condition. 
One must be careful, however, to exclude a relative mitral insuffi- 



VALVULAR LESIONS. 187 

ciency which, as has been already mentioned above, is very apt to 
supervene in cases of aortic disease, owing to dilatation of the mi- 
tral orifice, and which may modify the characteristic signs of aortic 
regurgitation very much as aortic stenosis does. 

TRICUSPID REGURGITATION. 

Endocarditis affecting the tricuspid valve is rare in post-fcetal 
life ; in the foetus it is not so uncommon. In cases of ulcerative 
or malignant endocarditis occuring in adult life, the tricuspid valve 
is occasionally involved, but the majority of cases of tricuspid dis- 
ease occur as a result of disease of the mitral valve and in the follow- 
ing manner : Hypertrophy of the right ventricle occurs as a result 
of the mitral disease, is followed in time by dilatation, and with 
this dilatation comes a stretching of the ring of insertion of the 
tricuspid valve, and hence a regurgitation through that valve. Tri- 
cuspid regurgitation, then, occurs in the latest stages of almost 
every case of mitral disease and sometimes during the severer at- 
tacks of failing compensation. 

Out of 405 autopsies at Guy's Hospital in which evidence of 
tricuspid regurgitation was found, 271, or two-thirds, resulted from 
mitral disease, 68 from myocardial degeneration, 55 from pulmonary 
disease (bronchitis, emphysema, cirrhosis of the lung). Very few of 
these cases had been diagnosed during life, and in all of them the 
valve was itself healthy but insufficient to close the dilated orifice. 

Gibson and some other writers believe that temporary tricuspid 
regurgitation is the commonest of all valve lesions, and results from 
weakening of the right ventricle in connection with states of anae- 
mia, gastric atony, fever, and many other conditions. It is very 
difficult to prove or disprove such an assertion. 

Tricuspid regurgitation is often referred to as serving like the 
opening of a " safety valve " to relieve a temporary pulmonary en- 
gorgement. This " safety-valve " action, however, may be most 
disastrous in its consequences to the organism as a whole, despite 
the temporary relief which it affords to the overfilled lungs. The 
engorgement is simply transferred to the liver and thence to the 



186 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

abdominal organs and the lower extremities, so that as a rule the 
advent of tricuspid regurgitation is recognized not as a relief but 
as a serious and probably fatal disaster. 

Physical Signs. 

(1) A systolic murmur is heard loudest at or near the fifth left 
costal cartilage. 

(2) Systolic venous pulsation in the jugulars and in the liver. 

(3) Engorgement of the right auricle producing an area of dul- 
ness beyond the right sternal margin. 

(4) Intense cyanosis. 

(1) The Murmur. — The maximum intensity of the systolic mur- 
mur of tricuspid regurgitation is usually near the junction of the fifth 
or sixth left costal cartilages with the sternum. Leube finds the 
murmur a rib higher up, but it is generally agreed that the tricuspid 
area is a large one, so that the murmur may be heard anywhere 
over the lower part of the sternum or even to the right of it. On the 
other hand, there are some tricuspid murmurs which are best heard 
at a point midway between the apex impulse and the ensif orm carti- 
lage. The murmur is not widely transmitted and is usually inaudi- 
ble in the back; at the end of expiration its intensity is increased. 

In some cases we have no evidence of tricuspid regurgitation 
other than the murmur just described, but — 

(2) Of more importance in diagnosis is the presence of a sys- 
tolic pulsation in the external jugular veins and of the liver, which 
unfortunately is not always present, but which when present is 
pathognomonic. I have already explained (see p. 35) the distinc- 
tion between true systolic jugular pulsation, which is practically 
pathognomonic of tricuspid regurgitation, and simple presystolic 
undulation or distention of the same veins, which has no necessary 
relation to this disease. The decisive test is the effort permanently 
to empty the vein by stroking it upward from below. If it in- 
stantly refills from below and continues to pulsate, tricuspid regur- 
gitation is almost certainly present. If, on the other hand, it does 
not refill from below, the cause must be sought elsewhere. 



VALVULAR LESIONS. 



189 



Pulsation in the liver must be distinguished from the "jogging " 
motion which may be transmitted to it from the abdominal aorta or 
from the right ventricle. To eliminate these transmitted impulses 
one must be able to grasp the liver bimanually, one hand in front 
and one resting on the lower ribs behind, and to feel it distinctly ex- 
pand with every systole, or else to take its edge in the hand and 
to feel it enlarge in one's grasp with every beat of the heart. 



Dilated right 
auricle. 



Systolic murmur. -"" 




Enlarged and pul- 
sating liver. 



Fig. 108.— Tricuspid Regurgitation. The murmur is heard hest over the shaded area. 



Pressure upon the liver often causes increased distention and pulsa- 
tion of the external jugulars if tricuspid regurgitation is present. 

(3) Enlargement of the heart, both to the right and to the left, 
as well as downward, can usually be demonstrated. In rare cases 
a dilatation of the right auricle may be suggested by a percussion 
outline such as that shown in Fig. 108. 

The pulmonic second sound is usually not accented. The im- 
portance of this in differential diagnosis will be mentioned pres- 
ently. If a progressive diminution in the intensity of the sound 
occurs under observation, the prognosis is very grave. 

(4) Cyanosis is usually very great, and dyspnoea and pulmonary 
oedema often make the patient's condition a desperate one. 



190 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Differential Diagnosis. 

The statistics of the cases autopsied at the Massachusetts Gen- 
eral Hospital show that tricuspid regurgitation is less often recog- 
nized during life than any other valvular lesion. The diagnosis 
was made ante mortem on only five out of twenty-nine cases. 
This is due to the following facts : 

(a) Tricuspid regurgitation may be present and yet give rise to 
no physical signs which can be recognized during life. 

(b) Tricuspid regurgitation occurs most frequently in connec- 
tion with mitral regurgitation; hence its signs are frequently 
masked by those of the latter lesion. It is, therefore, a matter of 
great importance as well as of great difficulty to distinguish tricus- 
pid regurgitation from 

(1) Mitral Regurgitation. 

The difficulties are obvious. The murmur of mitral regurgita- 
tion has its maximum intensity not more than an inch or two from 
the point at which the tricuspid murmur is best heard. Both are 
systolic in time. They are, therefore, to be distinguished only — 

(a) In case we can demonstrate that there are two areas in 
which a systolic murmur is heard with relatively great intensity, 
with an intervening space over which the murmur is less clearly to 
be heard (see Fig. 109). 

(b) Occasionally the two systolic murmurs are of different pitch 
or of different quality, and may be thus distinguished. 

(c) Tricuspid murmurs are not transmitted into the left axilla 
and are rarely audible in the back, and this fact is of value in case we 
have to distinguish between uncomplicated tricuspid regurgitation 
and uncomplicated mitral regurgitation. Unfortunately these le- 
sions are very apt to occur simultaneously, so that in practice our 
efforts are generally directed toward distinguishing between a pure 
mitral regurgitation and one complicated by tricuspid regurgitation. 

(d) In cases of doubt the phenomena of venous pulsation in the 
jugulars and in the liver are decisive if present, but their absence 
proves nothing. 



VALVULAR LESIONS. 



191 



(e) Accentuation of the pulmonic second sound is almost inva- 
riably present in uncomplicated mitral disease and is apt to disap- 
pear in case the tricuspid begins to leak, since engorgement of the 
lungs is thereby for the time relieved, but in many cases the pul- 
monic second sound remains most unaccountably strong even when 
the tricuspid is obviously leaking. 

(2) Erom " functional " systolic murmurs tricuspid insufficiency 
may generally be distinguished by the fact that its murmur is best 




Fig. 109.— Two Systolic Murmurs (Mitral and Tricuspid) with a tk Vanishing Point " between. 

heard in the neighborhood of the ensiform cartilage, and not in the 
second right intercostal space where most functional murmurs have 
their seat of maximum intensity. Functional murmurs are unac- 
companied by venous pulsation, cardiac dilatation, or cyanosis. 

(3) Occasionally a pericardial friction rub simulates the mur- 
mur of tricuspid insufficiency, but, as a rule, pericardial friction is 
much more irregular in the time of its occurrence and is not regu- 
larly synchronous with any definite portion of the cardiac cycle. 

Tricuspid Stenosis. 

One of the rarest of valve lesions is narrowing of the tricuspid 
valve. No case has come under my observation, and in 1898, Her- 



192 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

rick was able to collect but 154 cases from the world's literature. 
Out of these 154 cases, 138, or 90 per cent, were combined with 
mitral stenosis, and only 12 times has tricuspid stenosis been known 
to occur alone. 1 These observations account for the fact that tri- 
cuspid stenosis has hardly ever been recognized during life, since the 
murmur to which it gives rise is identical in time and quality and 
nearly identical in position with that of mitral stenosis. Narrow- 
ing of the tricuspid valve is to be diagnosed, therefore, only by the 
recognition of a presystolic murmur best heard in the tricuspid area 
and distinguished either by its pitch, quality, or position from the 
other presystolic murmur due to the mitral stenosis which is almost 
certain to accompany it. 

The heart is usually enlarged, especially in its transverse direc- 
tion, but the enlargement is just such as mitral stenosis produces, 
and does not aid our diagnosis at all. 

The diagnosis is still further complicated in many cases by the 
presence of an aortic stenosis in addition to .a similar lesion at the 
tricuspid and mitral valves, so that it seems likely that in the future 
as in the past the lesion will be discovered first at autopsy. 

Pulmonary Kegurgitation. 

Organic disease of the pulmonary valve is excessively rare in 
post-foetal life, but may occur as part of an acute ulcerative or 
septic endocarditis. A temporary functional regurgitation through 
the pulmonary valve may be brought about by any cause producing 
very high pressure in the pulmonary artery. I have known two 
medical students with perfectly healthy hearts who were able, by 
prolonged holding of the breath, to produce a short, high-pitched 
diastolic murmur best heard in the second and third left intercostal 
spaces and ceasing as soon as the breath was let out. Of the occur- 
rence of a murmur similarly produced under pathological condi- 
tions, especially in mitral stenosis, much has been written by 
Graham Steell. 

1 Out of 87 cases collected from the post-mortem records of Guy's Hos- 
pital, 85, or 97 per cent, were associated with still more extensive mitral 
stenosis, 



VALVULAR LESIONS. 193 

From the diastolic murmur of aortic regurgitation we may dis- 
tinguish the diastolic murmur of pulmonary incompetency by the 
fact that the latter is best heard over the pulmonary valve, is never 
transmitted to the apex of the heart nor to the great vessels, and 
is never associated with a Corrigan pulse nor with capillary pulsa- 
tion. 1 The right ventricle is hypertrophied, the pulmonic second 
sound is sharply accented and followed immediately by the murmur. 
Evidences of septic embolism of the lungs are frequently present 
and assist us in diagnosis. The regurgitation which may take 
place through the rigid cone of congenital pulmonary stenosis is 
not recognizable during life. 

Pulmonary Stenosis. 

Among the rare congenital lesions of the heart valves this is 
probably the commonest. The heart, and particularly the right 
ventricle, is much enlarged. There is a history of cyanosis and 
dyspnoea since birth. A systolic thrill is usually to be felt in the 
second left intercostal space, and a loud systolic murmur is heard 
in the same area. The pulmonic second sound is weak. 

The region in which this murmur is best heard has been happily 
termed the " region of romance " on account of the multiplicity of 
mysterious murmurs which have been heard there. The systolic 
murmur of pulmonary stenosis must be distinguished from 

(a) Functional murmurs due to anaemia and debility or to severe 
muscular exertion, and possibly associated with a dilatation of the 
Conus arteriosus. 

(b) Uncovering of the conus arteriosus through lack of expan- 
sion of the lung. 

(c) Aortic stenosis. 

(d) Mitral regurgitation. 

(e) Aneurism. 

(/) Roughening of the intima of the aortic arch. 

1 By registering the variations of pressure in the tracheal column of air 
Gerhardt has shown graphically that a systolic pulsation of the pulmonary cap- 
illaries may occur in pulmonary regurgitation. With the stethoscope a sys- 
tolic whiff may be heard all over the lungs. 

13 



194 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(a and b) Functional murmurs, and those produced in the conus 
arteriosus, are rarely if ever accompanied by a thrill, are rarely so 
loud as the murmur of pulmonary stenosis, and are not associated 
with dyspnoea, cyanosis, and enlargement of the right ventricle. 

(c) The murmur of aortic stenosis is usually upon the right side 
of the sternum and is transmitted to the neck, whereas the murmur 
of pulmonary stenosis is never so transmitted and is not associated 
with characteristic changes in the pulse (see above, p. 183). 

(d) The murmur of mitral regurgitation is occasionally loudest 
in the region of the pulmonary valve, but differs from the murmur 
of pulmonary stenosis in being, as a rule, transmitted to the back 
and axilla and associated with an accentuation of the pulmonary 
second sound. 

(e) Aneurism may present a systolic murmur and thrill similar 
to those found in pulmonary stenosis, but may usually be distin- 
guished from the latter by the presence of the positive signs of aneur- 
ism, viz. — pulsation, and dulness in the region of the murmur, and 
signs of pressure on the trachea or on other structures in the medi- 
astinum. 

(/) Roughening of the aortic arch occurs after middle life, 
while pulmonary stenosis is usually congenital. The murmur due 
to roughening may be transmitted into the carotids ; that of pul- 
monary stenosis never. Enlargement of the right ventricle is char- 
acteristic of pulmonary stenosis, but not of aortic roughening. 

COMBINED VALVULAR LESIONS. 

It is essential that the student should understand from the first 
that the number of murmurs audible in the precordia is no gauge 
for the number of valve lesions. We may have four distinct mur- 
murs, yet every valve sound except one. This is often the case in 
aortic regurgitation — systolic and diastolic murmurs at the base of 
the heart, systolic and presystolic at the apex, yet no valve in- 
jured except the aortic. In such a case the systolic aortic murmur 
is due to roughening of the aortic valve. The systolic apex mur- 
mur results from relative mitral leakage (with a sound valve). The 
presystolic apex murmur is of the " Flint " type. Hence in this 



VALVULAR LESIONS. 195 

case the diastolic murmur aloue of the four audible murmurs is due 
to a valvular lesiou. 

It is a good rule not to multiply causes unnecessarily, and to 
explain as many signs as possible under a single hypothesis. In 
the above example the mitral leak might be due to an old endocar- 
ditis, and there might be mitral stenosis and aortic stenosis as well, 
but since we can explain all the signs as results — direct and indirect 
— of one lesion (aortic regurgitation) it is better to do so, and post- 
mortem experience shows that our diagnosis is more likely to be 
right when it is made according to this principle. 

The most frequent combinations are : 

(1) Mitral regurgitation with mitral stenosis. 

(2) Aortic regurgitation with mitral regurgitation (with or with- 
out stenosis). 

(3) Aortic regurgitation with aortic stenosis, with or without 
mitral disease. 

(1) Double Mitral Disease. 

(a) It very frequently happens that the mitral valve is found 
to be both narrowed and incompetent at autopsy when only one of 
these lesions had been diagnosed during life. In fact mitral steno- 

lst 



Liil 



2nd 



! 



Fig. 110.— Mitral Stenosis and Regurgitation, showing relation of murmur to first heart sound. 

sis is almost never found at autopsy without an associated regurgi- 
tation, so that it is fairly safe to assume, whenever one makes the 
diagnosis of mitral stenosis, that mitral regurgitation is present as 
well, whether it is possible to hear any regurgitant murmur or not 
(see Fig. 110). 

(b) On the other hand, with a double mitral lesion one may 
have only the regurgitant murmur at the mitral valve and nothing 
to suggest stenosis unless it be a surprising sharpness of the first 
mitral sound. In chronic cases the changeableness of the murmurs 
both in type and position is extraordinary. One often finds at one 



196 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

visit evidences of mitral stenosis and at another evidences of mitral 
regurgitation alone. Either murmur may disappear altogether for 
a time and reappear subsequently. This is peculiarly true of the pre- 
systolic murmur, which is notoriously one of the most fleeting and 
uncertain of all physical signs. 

As a rule the same inflammatory changes which produce mitral 
regurgitation in early life result as they extend in narrowing the 
mitral valve, so that the signs of stenosis come to predominate in 
later years. Coincidently with this narrowing of the diseased valve 
a certain amount of improvement in the patient's symptoms may 
take place, and Kosenbach regards the advent of stenosis in such a 
case as an attempt at a regenerative or compensatory change. In 
many cases, however, no such amelioration of the symptoms follows. 

(2) Aortic Regurgitation with Mitral Disease. 

The signs of mitral disease occurring in combination with 
aortic regurgitation do not differ essentially from those of pure 



Systolic murmur 
over dilated- 
aortic arch. 




Maximum intensity 
and diastolic mur- 
mur, conducted 
up and down. 



■Systolic murmur. 



Fig. 111.— Aortic and Mitral Regurgitation. The shaded areas are those in which the murmurs 

are loudest. 



mitral disease except that the enlargement of the heart is apt to 
be more general and correspond less exclusively to the right ven- 
tricle (see Figs. Ill and 112). The manifestations of the aortic le- 



VALVULAR LESIONS. 197 

sion, on the other hand, are considerably modified by their associa- 
tion with the mitral disease. The Corrigan pnlse is distinctly less 
sharp at the summit and rises and falls less abruptly. Capillary 

1st 1st 

I III " 21u1 III 1 1 2nd 
llll lll l l I ll in i u m lllllliinii, llllm m 

Fig. 112.— Showing Relation of Murmurs to Heart Sound in Regurgitation at the Aortic and 

Mitral Valves. 

pulse is less likely to be present, and the throbbing of the peripheral 
arteries is less often visible. 

(3) Aortic Regurgitation with Aortic Stenosis. 

If the aortic valves are narrowed as well as incompetent, we 
find very much the same modification of the physical signs charac- 
teristic of aortic regurgitation as is produced by the advent of a 
mitral lesion ; that is to say, the throbbing in the peripheral ar- 
teries is less violent, the characteristics of the radial pulse are less 
marked, and the capillary pulsation is not always to be obtained 
at all. Indeed, this blunting of all the typical manifestations of 
aortic regurgitation may give us material aid in the diagnosis of 
aortic stenosis, provided always that the mitral valve is still per- 
forming its function. 

(4) The association of mitral disease with tricuspid insufficiency 
has been already described on p. 159. 



CHAPTER VIII. 

PAEIETAL DISEASE.— CARDIAC NEUROSES.— CONGENI- 
TAL MALFORMATIONS OF THE HEART. 

Parietal Disease of the Heart. 
Acute Myocarditis. 

The myocardium is seriously, though not incurably, affected in 
all continued fevers, owing less to the fever itself than to the tox- 
aemia associated with it. "Cloudy swelling," or granular degener- 
ation of the muscle fibres, is produced by relatively mild infections, 
while a general septicaemia due to pyogenic organisms may produce 
extensive fatty degeneration of the heart within a few days. 

The physical signs are those of cardiac weakness. The most 
significant change is in the quality of the first sound at the apex 
of the heart, which becomes gradually shorter and feebler until its 
quality is like that of the second sounds, while its feebleness makes 
the second sounds seem accented by comparison. Soft blowing 
systolic murmurs may develop at the pulmonary orifice, less often 
at the apex or over the aortic valve. 

The apex impulse becomes progressively feebler and more like 
a tap than a push. Irregularity and increasing rapidity are omi- 
nous signs which may be appreciated in the radial pulse, but still 
better by auscultation of the heart itself. In most of the acute in- 
fections evidence of dilatation of the weakened cardiac chambers is 
rarely to be obtained during life (although at autopsy it is not in- 
frequently found), 1 but in acute articular rheumatism an acute dila- 
tation of the heart appears to be a frequent complication, independ- 

1 Hencken's recent monograph on this subject, "Ueberdie acute Herzdila- 
tation bei acuten Infectionskrankheiten," Jena, 1899, does not seem to me 
convincing. 



PARIETAL DISEASE. 199 

ent of the existence of any valvular disease. Attention has been 
especially called to this point by Lees and Boynton (British Med. 
Jour., July 2, 1898) and by S. West. 

Influenza is also complicated not infrequently by acute cardiac 
dilatation. 

Chronic Myocarditis (" Weakened Heart "). 

Fatty or fibroid changes in the heart wall occurring in chronic 
disease are usually the result of sclerosis of the coronary arteries 
and imperfect nutrition of the myocardium, but chronic toxaemias, 
like pernicious anaemia, may also produce a very high grade of fatty 
degeneration of the heart and especially of the papillary muscles. 

Whether fatty or fibroid changes predominate, the physical signs 
are the same. 

Physical Signs of Chronic Myocarditis. 

For the recognition of these changes in the myocardium our 
present methods of physical examination are always unsatisfactory 
and often wholly inadequate. Extensive degenerations of the 
heart wall are not infrequently found at autopsy when there has 
been no reason to suspect them during life. On the other hand, 
the autopsy often fails to substantiate a diagnosis of degeneration 
of the heart muscle, although all the physical signs traditionally 
associated with this condition were present during life. 1 To a con- 
siderable extent, therefore, our diagnosis of myocarditis must de- 
pend upon the history and symptoms of the case ; physical exami- 
nation can sometimes supplement these, sometimes not. Symptoms 
of cardiac weakness developing in a man past middle life, especially 
in a patient who shows evidences of arterio-sclerosis or high ar- 
terial tension, or who has suffered from the effects of alcohol and 
syphilis, suggest parietal disease of the heart, fatty or fibroid. 
The probability is increased if there have been attacks of angina 
pectoris, Cheyne-Stokes breathing, or of syncope. 

Inspection and palpation may reveal nothing abnormal, or there 

1 A well-known Boston pathologist recently told me that he had never 
known a case of myocarditis correctly diaguosed during life. 



200 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

may be an unusually diffuse, slapping cardiac impulse associated 
perhaps with a displacement of the apex beat to the left a,nd down- 
ward. Marked irregularity of the heart beat, both in force and in 
rhythm, is sometimes demonstrable by these methods, and an in- 
crease in the area of cardiac dulness may be demonstrable in case 
dilatation has followed the weakening of the heart wall. Ausculta- 
tion may reveal nothing abnormal except that the aortic second 
sound is unusually sharp ; in some cases feeble and irregular heart 
sounds are heard, although the first sound at the apex is not infre- 
quently sharp. Ee duplication of one or both sounds and disturb- 
ance of rhythm, especially the "gallop rhythm," are not infre- 
quent. If the mitral sphincter is dilated, or the papillary muscles 
are weakened, as not infrequently happens, we may have evidences of 
mitral regurgitation, a systolic murmur at the apex heard in the left 
axilla and back with accentuation of the pulmonic second sound. 

Summary. 

1. The history and symptoms of the case or the condition of 
other organs are often of more diagnostic value than is the physical 
examination of the heart itself, which may show nothing abnormal. 

2. Among the rather unreliable physical signs, those most often 
mentioned are : 

(a) Weakness and irregularity of the heart sounds. 

(b) Accentuation of the aortic second sound. 

(c) A diffuse slapping cardiac impulse. 

(d) Keduplication of some of the cardiac sounds (gallop 
rhythm). 

(e) Evidences of cardiac dilatation. 

(/) Murmurs— especially the murmur of mitral insufficiency 
which often occurs as a result of dilatation of the valve orifices and 
weakening of the cardiac muscle. 

Differential Diagnosis. 
We have to distinguish myocarditis from — 

(a) Uncomplicated valvular lesions. 

(b) Cardiac neuroses. 



PARIETAL DISEASE. 201 

(a) It has been already pointed ont that valvular lesions do not 
necessarily give rise to any murmurs when compensation has failed. 
Under such circumstances one hears only irregular and weak heart 
sounds, as in myocarditis. The history of a long-standing valvu- 
lar trouble, a knowledge of the previous existence of murmurs, the 
age, method of onset, and symptoms of the case may assist us in 
the diagnosis. Cases of myocarditis are less likely to be associated 
with extensive dropsy than are cases of valvular disease whose com- 
pensation has been ruptured. 

(b) Weakness and irregularity of the cardiac sounds, when due 
to nervous affection of the heart and unassociated with parietal or 
valvular changes, is usually less marked after slight exertion. The 
heart "rises to the occasion" if the weakness is a functional one. 
On the other hand, if fatty or fibroid changes are present, the signs 
and symptoms are much aggravated by any exertion. 

In some cases of myocarditis the pulse is excessively slow and 
shows no signs of weakness. This point will be referred to again 
in the chapter on Bradycardia. 

Fatty Overgrowth. 

An abnormally large accumulation of fat about the heart may 
be suspected if, in a very obese person, signs of cardiac embarrass- 
ment (dyspnoea, palpitation) are present, and if on examination we 
find that the heart sounds are feeble and distant but preserve the 
normal difference from each other. When the heart wall is seri- 
ously weakened (as in the later weeks of typhoid), the heart sounds 
become more alike owing to the shortening of the first sound. 

In fatty overgrowth this is not the case. 

The diagnosis, however, cannot be positively made. We sus- 
pect it under the conditions above described, but no greater cer- 
tainty can be attained. 

Fatty Degeneration. 

There are no physical signs by which fatty degeneration of the 
heart can be distinguished from other pathological changes which 
result in weakening the heart walls. An extensive degree of fatty 



202 PHYSICAL DIAGNOSIS OF DISEASES OF TEE CHEST, 

degeneration is often seen post mortem in cases of pernicious anaemia, 
although the heart sounds have been clear, regular, and in all re- 
spects normal during life. The little we know of the physical 
signs common to fatty degeneration and to other forms of parietal 
disease of the heart has been included m the section on Myocar- 
ditis (see p. 198), 

Cardiac Neuroses. 
Tachycardia (Rapid Heart). 

Simple quickening of the pulse rate, or tachycardia, which may 
pass altogether unnoticed by the patient himself, is to be distin- 
guished from palpitation, in which the heart beats, whether rapid 
or not, force themselves upon the patient's attention. 

The pulse rate may vary a great deal in health. A classmate 
of mine at the Harvard Medical School had a pulse never slower 
than 120, yet his heart and other organs were entirely sound. Such 
cases are not very uncommon, especially in women. Temporarily 
the pulse rate may be greatly increased, not only by exercise and 
emotion, but by the influence of fever, of gastric disturbances, or of 
the menopause. Such a tachycardia is not always of brief duration. 
The effects of a great mental shock may produce an acceleration of 
the pulse which persists for days or even weeks after the shock. 

Among organic diseases associated with weakening of the pulse 
the commonest are those of the heart itself. Next to them, exoph- 
thalmic goitre, tumors or hemorrhage in the medulla, and obscure 
diseases of the female organs of generation, are the most frequent 
causes of tachycardia. 

The only form of tachycardia which is worthy to be considered 
as a more or less independent malady is 

Pa roxys mal Ta eh yea rd i a . 

As indicated in the name, the attacks of this disease are apt to 
begin and to cease suddenly. They may last a few hours or several 
days. The pulse becomes frightfully rapid, often 200 per minute or 
more. Bristowe records a case with a pulse of 308 per minute. 



CARDIAC NEUROSES. 203 

In the radial artery tlie pulse beat may be impalpable. The heart 
sounds are regular and clear, but the diastolic pause is shortened and 
the first sound becomes short and "valvular," resembling the sec- 
ond ("tic-tac heart"). The paroxysm may be associated with 
aphasia and abnormal sensations in the left arm. Occasionally the 
heart becomes dilated, and oedema of the lungs, albuminuria, and 
other manifestations of stasis appear. As a rule, however, paroxys- 
mal tachycardia can be distinguished from the rapid heart-beat 
associated with cardiac dilatation by the fact that the heart remains 
perfectly regular. This same fact also assists us in excluding the 
cardiac neuroses due to tobacco, tea, and other poisons. From the 
tachycardia of Graves' disease the affection now in consideration 
differs by its paroxysmal and intermittent character. 

Bradycardia (Slow Heart). 

In many healthy adults the heart seldom beats over 50 times a 
minute. 

I. Among the causes which may produce for a short time an 
abnormally slow heart-beat are : 

(a) Exhaustion; for example, after fevers, after parturition, or 
severe muscular exertion. 

(b) Toxaemia; for example, jaundice, uraemia, auto-intoxications 
in dyspepsia. 

(c) In certain hysterical and melancholic states and in neurotic 
children, the pulse may be exceedingly slow. Pain has also a ten- 
dency to retard the pulse. 

(d) An increase of intracranial pressure, as in meningitis, cere- 
bral hemorrhage, depressed fracture of the skull. Possibly in this 
category belong the cases of bradycardia sometimes seen in epilep- 
tiform or during syncopal attacks. Bradycardia from any one of 
these causes is apt to be of comparatively short duration. 

II. Permanent bradycardia is most often associated with coro- 
nary sclerosis and myocarditis. In this disease the pulse may re- 
main below 40 for months or years, though strong and regular, yet 
the patient may be free from disagreeable symptoms of any kind. 
The rate of the heart-beat cannot always be estimated by counting 



204 PHYSICAL DIAGNOSIS OF DISEASES OF TEE CHEST. 

the radial pulse. Not infrequently many pulsations of the heart 
are not of sufficient force to transmit a wave to the radial artery, 
and the mistake should never be made of diagnosing bradycardia 
simply by counting the radial pulse. 

Arrhythmia. 

1 . Physiological Arrhythmia. — Arrhythmia, or irregularity in the 
force or rhythm of the heart-beat, is to a certain extent physiologi- 
cal. The heart normally beats a little faster and a little more strongly 
during inspiration than during expiration. Any psychical disturb- 
ance or muscular exertion may produce irregularity as well as a 
quickening of the heart-beat. Rarely the pulse may be irregular 
throughout life in perfectly healthy persons/ This irregularity is 
usually of rhythm alone ; every second or third beat may be regu- 
larly omitted without the individual knowing anything about it or 
feeling any disagreeable symptoms connected with it. More rarely 
the heart's beats may be permanently irregular in force as well as 
rhythm despite the absence of any discoverable disease. 

In children the pulse is especially apt to be irregular, and dur- 
ing sleep some children show that modification of rhythm known 
as the "paradoxical pulse," which consists in a quickening of the 
pulse with diminution in volume during inspiration. 

(2) If we leave on one side diseases of the heart itself, patho- 
logical arrhythmia is most frequently seen in persons who have used 
tobacco or tea to excess, or in dyspepsia. In these conditions it is 
often combined with palpitation and becomes thereby very distress- 
ing to the patient. In connection with cardiac disease the follow- 
ing types of arrhythmia may be distinguished : 

(a) Paradoxical Pulse. — Any cause which leads to weakening 
of the heart's action may occasionally be associated with paradoxical 
pulse. Fibrous pericarditis has been supposed to be frequently 
associated with this type of arrhythmia, but if so it is by no means 
its only cause. 

(b) The bigeminal pulse is seen most frequently in cases of un- 
compensated heart disease (particularly mitral stenosis) after the 
administration of digitalis. Every other beat is weak or abortive 



CARDIAC NEUROSES. 205 

and is succeeded by an unusually long pause. Sometimes every 
third beat is of the abortive type, or an unusually long interval 
may divide the heart-beats into groups of three ("trigeminal 
jiulse"). 

(c) Embryocardla, or the "tic-tac heart," represents a shorten- 
ing of the diastolic pause and of the first sound of the heart so that 
it resembles the second sound, as in the foetal heart. Any case of 
uncompensated heart disease, whether valvular or parietal, may be 
associated with this disturbance of rhythm. 

(d) The gallop rhythm. 

Owing to a reduplication of one of the heart sounds (usually 
the second), we may have three sounds instead of two with each 
beat of the heart, the sounds possessing a rhythm which reminds us 
of the hoof -beats of a galloping horse (see p. 123). This rhythm is 
heard especially in the failing heart of interstitial nephritis or cor- 
onary sclerosis. 

(e) Delirium cordis is a term used to express any great irregu- 
larity and rapidity of the heart-beats which cannot be reduced to 
a single type or rhythm. It is seen in the gravest stages of uncom- 
pensated heart disease. 

Palpitation. 

Defined by Osier as " irregular or forcible heart action percep- 
tible to the individual " The essential point is that the individual 
becomes conscious of each beat of his heart, whether or no the heart 
action is in any way abnormal. 

(a) In irritable conditions of the nervous system, such as occur 
at puberty, at climacteric, or in neurasthenic persons, palpitation 
may be very distressing. Temporary disturbances, such as fright, 
may produce a similar and more or less lasting effect. 

(b) The effect of high altitudes, or of even a moderate eleva- 
tion (1,500 feet) is sufficient to produce in many healthy persons a 
quickening and strengthening of the heart's action, so that sleep 
may be prevented. After a few nights this condition usually 
passes off, provided the heart is sound. 

(c) Abuse of tobacco and tea have a similar effect. 



206 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Auscultation of a palpitating heart shows nothing more than 
unusually loud and ringing heart sounds, but since palpitation is 
often associated with arrhythmia of one or another type we must be 
careful to exclude the palpitation symptomatic of acute dilatation 
of the heart, such as may occur in debilitated persons after violent 
or unusual exertion. In this condition the area of cardiac dulness 
is increased and dyspnoea upon slight exertion becomes marked. It 
goes without saying that in almost any case of organic disease of 
the heart palpitation may be a very marked and distressing symp- 
tom. 

CONGENITAL HEAKT DISEASE. 

From the time of birth it is noticed that the child is markedly 
and permanently cyanosed, hence the term "blue baby." Dyspnoea 
is often, though not always, present, and may interfere with suck- 
ing. The cyanosis is practically sufficient in itself for the diag- 
nosis. 

Among congenital diseases of the heart the commonest and the 
most important (because it is less likely than any of the others to 
prove immediately fatal) is : 

1. Pulmonary Stenosis. 

This lesion is usually the result of foetal endocarditis, and is 
often associated with malformations and defects, such as patency 
of the foramen ovale and persistence of the ductus arteriosus. The 
physical signs of pulmonary stenosis are : 

(a) A palpable systolic thrill most distinct in the pulmonary 
area. 

(b) A loud murmur (often rough or musical) heard best in the 
same region, but usually transmitted to all parts of the chest. 

(c) A weak or absent pulmonic second sound. 

(d) An increased area of cardiac dulness corresponding to the 
right ventricle. 

Unlike most other varieties of congenital heart disease, pulmo- 
nary stenosis is compatible with life for many years, and "blue 
babies " with this lesion may grow up and enjoy good health, al- 



CONGENITAL HEART DISEASE. 207 

though usually subject to pulmonary disorders (pneumonia or tu- 
berculosis). For a discussion of the differential diagnosis of this 
lesion, see above, p. 193. 

2. Defects in the Ventricular Septum. 

The loud systolic murmur produced by the rush of blood through 
an opening between the ventricles is heard, as a rule, over the whole 
precordia. Its point of maximum intensity differs in different 
cases, but is hardly ever near the apex of the heart. The most im- 
portant diagnostic point is the absence of a palpable thrilL With 
almost every other form of congenital heart disease in which a loud 
murmur is audible, there is a thrill as well Hypertrophy of both 
ventricles may be present, but is seldom marked in uncomplicated 
cases. 

{Patency of the foramen ovale, if unassociated with other de- 
fects, does not usually produce any murmur or other signs by which 
it can be recognized during life, and causes no symptoms of any 
kind.) 

3. Persistence of the Ductus Arteriosus. 

The most characteristic sign is a loud, vibratory systolic mur- 
mur with its intensity at the base of the heart and unassociated with 
hypertrophy of either ventricle. If complicated with stenosis at or 
close above the pulmonary valves, persistence of the ductus arte- 
riosus cannot be diagnosed, as the murmur produced by it cannot 
with certainty be distinguished from that of the pulmonary ste- 
nosis, and the presence of hypertrophy of the right ventricle de- 
prives us of the one relatively characteristic mark of a patent arte- 
rial duct. 

It has been claimed that a murmur persisting through systole 
and into diastole is diagnostic of an open arterial duct, but this 
supposition is not borne out by post-mortem evidence. 

The signs produced by the other varieties of congenital heart 
disease, such as aortic stenosis and tricuspid or mitral lesions, do 
not differ materially from those characterizing those lesions hi 



208 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

adults. Excluding these, we may summarize the signs of the other 
lesions as follows : 

(a) Practically all cases of congenital heart disease, which pro- 
duce any physical signs beyond cyanosis and dyspnoea, manifest 
themselves by a loud systolic murmur heard all over the precordia 
and often throughout the chest. Its maximum intensity is usually 
at or near the base of the heart. 

(b) If there is no thrill and no hypertrophy, the lesion is prob- 
ably a defect in the ventricular septum. 

(c) If there is a thrill but no hypertrophy, the lesion is probably 
a patent ductus arteriosus. 

(d) If there is a thrill and hypertrophy of the right ventricle, 
the lesion is probably pulmonic stenosis, especially if the pulmonic 
second sound is feeble. 



CHAPTER IX. 

DISEASES OF THE PEKICAKDIUM. 

I. Pericarditis. 

Three forms are recognized clinically : 

(1) Plastic, dry, or fibrinous pericarditis. 

(2) Pericarditis with, effusion (serous or purulent). 

(3) Pericardial adhesions or adherent pericardium. 
Fibrinous pericarditis may be fully developed without giving 

rise to any physical signs that can be appreciated during life. In 
several cases of pneumonia in which I suspected that pericarditis 
might be present, I have listened most carefully for evidences of 
the disease and been unable to discover any ; yet at autopsy it was 
found fully developed — the typical shaggy heart. We have every 
reason to believe, therefore, that pericarditis is frequently present 
but unrecognized, especially in pneumonia and in the rheumatic at- 
tacks of children. On the other hand, it may give rise to very 
marked signs which are the result of — 

(a) The rubbing of the roughened pericardial surfaces against 
one another when set in motion by the cardiac contractions. 

(b) The presence of fluid in the pericardial sac. 

(c) The interference with cardiac contractions brought about by 
obliteration of the pericardial sac together with the results of ad- 
hesions between the pericardium and the surrounding structures. 

(1) Dry or Fibrinous Pericarditis. 

The diagnosis rests upon a single physical sign — "pericardial 

friction " — which is usually to be appreciated by auscultation alone, 

but may occasionally be felt as well. Characteristic pericardial 

friction is a rough, irregular, grating or shuffling sound which oc- 

14 



210 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

curs irregularly and interruptedly during the larger part of each 
cardiac cycle. It is almost never accurately synchronous either 
with systole or diastole, but overlaps the cardiac sounds, and en- 
croaches upon the pauses in the heart cycle. It is seldom exactly 
the same in any two successive cardiac cycles and differs thereby 
from sounds produced within the heart itself. Pericardial friction 
seems very near to the ear and may often be increased by pressure 




Pericardial f fiction. 



Fig. 113.— Showing Most Frequent Site of Audible Pericardial Friction. 



with the stethoscope ; it is not materially influenced by the respi- 
ratory movements. 

It is best heard in the majority of cases in the position shown 
in Fig. 113 ; that is, over that portion of the heart which lies near- 
est to the chest wall and is not covered by the margins of the lungs ; 
but not infrequently it may be heard at the base of the heart or 
over the whole precordial region. The sounds are fainter if the 
patient lies on the right side, and sometimes intensified if, while 
sitting or standing, he leans forward and toward the left, so as to 
bring the heart into closer apposition with the chest wall. 

Pericardial friction sounds often change rapidly from hour 
to hour, and may disappear and reappear in the course of a 
day. 



DISEASES OF THE PERICARDIUM. 211 

In rare cases the friction may occur only during systole or only 
during diastole. In such cases the diagnosis between pericardial 
and intracardial sounds may be very difficult. 

Differential Diagnosis. 

(a) PI euro- Pericardial Friction. 

Fibrinous inflammation affecting that part of the pleura which 
overlaps the heart may give rise to sounds altogether indistinguish- 
able from those of true pericardial friction when the inflamed pleu- 
ral surfaces are made to grate against one another by the move- 
ments of the heart. Such sounds are sometimes increased in 
intensity during forced respiration and disappear at the end of 
expiration, while true pericardial friction is usually best heard if 
the breath is held at the end of expiration. If a friction sound 
heard in the pericardial region ceases altogether when the breath 
is held, Ave may be sure that it is produced in the pleura and not 
in the pericardium, but in many cases the diagnosis cannot be made 
correctly. 

(b) Intracardiac Murmurs. 

From murmurs due to valvular disease of the heart, pericardial 
friction can usually be distinguished by the fact that the sounds to 
which it gives rise do not accurately correspond either with systole 
or diastole, and do not occupy constantly any one portion of either 
of these periods. Cardiac murmurs are more regular, seem less 
superficial, and vary less with position and from hour to hour. 
Pressure with the stethoscope does not increase so considerably the 
intensity of intracardiac murmurs. When endocarditis and peri- 
carditis occur simultaneously, it may be very difficult to distinguish 
the two sets of sounds thus produced. The pericardial friction is 
usually recognized with comparatively little difficulty, but it is 
hard to make sure whether in addition we hear endocardial mur- 
murs as well. 



212 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



(2) Pericardial Effusiox. 

Following the fibrinous exudation, which roughens the pericar- 
dial surface and produces the friction sounds just described, serum 
may accumulate in the pericardial sac. Its quantity may exceed 
but slightly the amount of fluid normally present in the pericar- 
dium, or may be so great as to embarrass the cardiac movements 
and finally to arrest them altogether. In chronic (usually tubercu- 
lous) cases, the pericardium may become stretched so as to hold a 
quart or more without seriously interfering with the heart's action, 
while a much smaller quantity, if effused so rapidly that the peri- 
cardium has no time to accommodate itself by stretching, will prove 
rapidly fatal. 

Hydropericardium denotes a dropsy of the pericardium occur- 
ring by transudation as part of a general dropsy in cases of renal 
disease or cardial weakness. The physical signs to which it gives 
rise do not differ from those of an inflammatory effusion, and, ac- 
cordingly, all that is said of the latter in the following section may 
be taken as equally an account of the signs of hydropericardium. 

Hsemopericardium, or blood in the pericardial sac, due to stabs 
or to ruptures of the heart, is usually so rapidly fatal that no 
physical signs are recognizable. 

Physical Signs of Pericardial Effusion. 

In most cases a pericardial friction rub has been observed prior 
to the time of the fluid accumulation. The presence of fluid in the 
pericardial sac is shoivn chiefly in three ways : 

(1) By percussion, which demonstrates an area of dulness more 
or less characteristic (see below). 

(2) By auscultation, which may reveal an unexpected feebleness 
in the heart sounds when compared with the power shown in the 
radial pulse. 

(3) By the signs and symptoms of pressure exerted by the peri- 
cardial effusion upon surrounding structures. 

Bulging of the precordia is occasionally to be seen in children ; 



DISEASES OF THE PERICARDIUM. 213 

in adults we sometimes observe a flattening of the interspaces just 
to the right of the sternum between the third and sixth ribs. 

(1) The Area of Percussion Dulness. — (a) One of the most char- 
acteristic points is the unusual 1 extension of the percussion dulness 
a considerable distance to the left and beyond the cardiac impulse. 
(b) Next to this, it is important to notice a change in the angle 
made by the junction of the horizontal line corresponding to the 
upper limit of hepatic dulness and the nearly perpendicular line 
corresponding to the right border of the heart. In health this 



Tympany, 




_-\--- Dulness, 



~ ' Cardiac impulse. 



Liver dulness. -' 



Fig. 114.— Percussion Dulness in Pericardial Effusion, with Tympanitic Resonance Under the 

Left Clavicle. 

cardio-hepatic angle is approximately a right angle ; in pericardial 
effusion it is much more obtuse (see Fig. 114). Rotch has called 
attention to the importance of dulness in the fifth right intercostal 
space as a sign of pericardial effusion, but a similar dulness may be 
produced by enlargement of the liver. 

Except for the two points mentioned above (the unusual extension 
of the dulness to the left of the cardiac impulse and the blunting of 
the cardio-hepatic angle), there seems to me to be nothing charac- 
teristic about the area of dulness produced by pericardial friction. 

1 In health the cardiac dulness extends about three- fourths of an inch be- 
yond the cardiac impulse, but in pericardial effusion the difference is greater. 



214 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

The " pear-shaped " or triangular area of percussion dulness men- 
tioned by many writers has not been present in cases which have 
come under my observation. In large effusions percussion reso- 
nance may be diminished in the left back, and under the left clav- 
icle the percussion note may be tympanitic from relaxation of the 
lung. Traube's semilunar space may be obliterated, but this occurs 
also in pleuritic effusions. 

In some cases the area of dulness may be modified by change in 
the patient's position. After marking out the area of percussion 
dulness with the patient in the upright position, let him lie upon 
his right side. The right border of the area of dulness will some- 
times move considerably farther to the right. A dilated heart can 
be made to shift in a similar way, but to a lesser extent. Compar- 
atively little change takes place if the patient lies on his left side, 
and no important information is elicited by placing him flat on his 
back or by getting him to lean forward. 

Unfortunately, it is only with moderate-sized effusions occur- 
ring in a pericardial sac free from adhesions to the surrounding 
parts that this shifting can be made out. Large effusions may not 
shift appreciably, and less than 150 c.c. of fluid probably cannot be 
recognized by this or by any other method. But with large effu- 
sions the lateral extension of the area of dulness may be so great 
as to be almost distinctive in itself, i.e., from the middle of the left 
axilla nearly to the right nipple. 

(2) The feebleness of the heart sounds, especially those at the 
apex, is of diagnostic importance only in the rare cases when it oc- 
curs in connection with a relatively normal condition of the radial 
pulse. In most diseases feeble heart sounds are associated with a 
weak pulse, but occasionally in pericardial effusion the pulse may 
be of good quality, although the heart sounds are heard with diffi- 
culty. 

Broncho-vesicular breathing with increased voice sounds may 
be heard over the tympanitic area below the left clavicle and occa- 
sionally between the scapulae behind. This is a result of compres- 
sion of the lung. 

(3) Pressure exerted by the pericardial exudation upon sur- 



DISEASES OF THE PERICARDIUM. 215 

rounding structures may give rise to dyspnoea, especially of a 
paroxysmal type, to dysphagia, to aphonia, and to an irritating 
cough. The "paradoxical pulse," small and feeble during inspira- 
tion, is occasionally to be seen, but is by no means peculiar to this 
condition and has no considerable diagnostic importance. 

(4) Inspection and palpation usually help us very little, but two 
points are occasionally demonstrable by these methods : 

(a) A smoothing out of the intercostal depression in the precor- 
dial region, especially near the right border of the sternum between 
the third and the sixth ribs. 

(b) A progressive diminution of the intensity of the apex im- 
pulse until it may be altogether lost, If this change occurs while 
the patient is under observation, and especially if the apex impulse 
reappears or becomes more distinct when the patient lies on the 
right side, it is of considerable diagnostic value. In conditions 
other than pericardial effusion, the apex impulse becomes less visible 
in the right-sided decubitus. 

Differential Diagnosis. 

(1) Our chief difficulty is to distinguish the disease from hyper- 
trophy and dilatation of the heart. In the latter, which often com- 
plicates acute articular rheumatism with or without plastic pericar- 
ditis, the apex impulse is often very indistinct to sight and touch 
as in pericardial effusion. But the area of dulness is less likely to 
extend beyond the apex impulse to the left or to modify the cardio- 
hepatic angle, or to shift when the patient lies on the right side. 
Pressure symptoms are absent, and there are no areas of broncho- 
vesicular breathing with tympanitic resonance under the left clavicle 
or in the axilla. Yet not infrequently these differentise do not 
serve us, and the diagnosis can be made only by puncture. 

(2) I have twice known cases of encapsulated empyema mistaken 
for pericardial effusion. In one case a needle introduced in the 
fifth intercostal space below the nipple drew pus from what turned 
out later to be a localized purulent pleurisy, but the diagnosis was 
not made until a rib had been removed and the region thoroughly 
explored. It is not rare for pleuritic effusions to gather first 



216 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

iii this situation, viz., just outside the apex impulse in the left 
axilla. 

Such effusions may gravitate very slowly to the bottom of the 
pleural cavity or may become encapsulated and remain in their 
original and very deceptive position. In such cases the signs of 
compression of the left lung are similar to those produced by a 
pericardial effusion, and the results of punctures may be equivocal 
as in the case just mentioned. If there is any dulness, even a very 
narrow zone, in the left axilla between the fifth and eighth ribs, 
though there be none in the back, the likelihood of pleurisy should 
be suggested. 

As between pleuritic and pericardial effusion the presence of a 
good pulse and the absence of marked dyspnoea favors the former. 
In the two cases above referred to in which encapsulated pleurisy 
was mistaken for pericarditis, the general condition of the patient 
struck me at the time as surprisingly good for pericarditis. 

If both pleurisy and pericarditis are present, the area of peri- 
cardial dulness is not characteristic until the pleuritic fluid has been 
drawn off. The persistence of dulness in the cardio-hepatic angle 
and beyond the apex beat after a left pleurisy has been emptied by 
tapping, and after the heart has had time to return to its normal 
position, should make us suspect a pericardial effusion. 

Despite the utmost care and thoroughness in physical examina- 
tion, many cases of pericardial effusion go unrecognized, especially 
in infants, in elderly persons, or when the lung borders are adher- 
ent to the pericardium or to the chest wall. 

In the rheumatic attacks of children, it should be remembered 
that pericarditis is even more common than endocarditis. 

Adherent Pericardium. 

In the majority of cases the diagnosis cannot be made during 
life, unless the pericardium is adherent, not only to the heart, but 
to the walls of the chest as well. When this combination of peri- 
carditis with chronic mediastinitis is present, the diagnosis may be 
suggested by 

(ft) A systolic retraction of the chest wall in the region of the 



DISEASES OF THE PERICARDIUM. 217 

apex impulse at the base of the left axilla and in the region of the 
eleventh and twelfth ribs in the left back (Broadbent's sign). Such 
retraction is more marked during a deep inspiration. (It should 
be remembered that systolic retraction of the interspaces in the 
vicinity of the apex is very commonly seen in cases of cardiac hy- 
pertrophy from any cause, owing to the negative pressure produced 
within the chest by the contraction of a powerful heart.) A quick 
rebound of the cardiac apex at the time of diastole (the diastolic 
shock) is said to be characteristic of pericardial adhesions, but is 
often absent. 

(b) Collapse of the cervical veins during diastole has been no- 
ticed by Friedreich, and the paradoxical pulse, above described, is 
said to be more marked in adherent pericardium than in any other 
known condition. Most recent writers, however, place no reliance 
upon it. 

(c) When the lungs are adherent to the pericardium or to the 
chest wall, as is not uncommonly the case, the absence of the phrenic 
phenomenon (Litten's signs) and of any respiratory excursion of 
the pulmonary margins may be demonstrated. Since pericardial 
adhesions are most often due to tuberculosis, the discovery of tu- 
berculosis in the lung or elsewhere may be of aid in diagnosis. 

(d) Broadbent considers that the absence of any shift in the 
position of the apex beat, with respiration or change of patient's 
position, is an important point in favor of mediastino-pericarditis. 
In health and in valvular or parietal disease of the heart, the apex 
beat will swing from one to two inches to the left when the patient 
lies on his left side, and the descent of the diaphragm during full 
inspiration lowers the position of the cardiac impulse considerably. 

(e) The presence of hypertrophy or dilatation affecting espe- 
cially the right side of the heart, and not accounted for by the 
existence of any disease of the cardiac valves, of the lung, or of 
the kidney, should make us suspect pericardial and mediastinal 
adhesions. Such adhesions embarrass especially the right ven- 
tricle, because it is the right ventricle far more than the left which 
becomes attached to the chest wall. The left ventricle is more 
nearly free. 



218 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



(/) Since the space enclosed by the divergent costal cartilage 
just below the ensiform is but loosely associated with the cen- 
tral tendon of the diaphragm, Broadbent looks especially at this 



■ * 4 



/ 



. 




n 



'■* 



Fig. 115. 







Fig. 116. 



Figs. 115, 116.— Adherent Pericardium, Ascites. 

point for evidence of mediastinal or pericardial adhesions, the 
effect of which is to arrest completely the slight respiratory move- 
ments of this part of the abdominal wall. 

(g) Adherent pericardium, occurring as a part of a widespread 



DISEASES OF THE PERICARDIUM. 219 

chain of fibrous processes involving the pleura, the mediastinum, 
and the peritoneum, may give rise in young persons to a train of 
symptoms and signs suggesting cirrhosis of the liver. Ascites 
collects, the liver is enlarged, yet there are no signs in the heart, 
kidneys, or blood sufficient to explain the condition. In any such 
case adherent pericardium should be considered. Figs. 115 and 116 
show the appearance in cases of this kind in which the diagnosis 
was verified by autopsy. 

Summary. 

The diagnosis of adherent pericardium with chronic mediastini- 
tis is suggested by 

(«) Systolic retraction of the lower intercostal spaces in the 
left axilla and in the left back, followed by a diastolic rebound. 

(I)) The absence of any change in the position of the apex im- 
pulse with respiration or change of position. 

(c) The presence of hypertrophy and dilatation of the right 
ventricle without obvious cause. 

(d) The absence of any respiratory excursion of the lung bor- 
ders near the heart and of the abdominal wall at the costal angle. 

(e) The presence of signs like those of hepatic cirrhosis in a 
young person and without any obvious cause. 



CHAPTER X. 

THOEACIC ANEUKISM. 
Aneurism of the Thoracic Aorta. 

For clinical purposes thoracic aneurisms may be divided into 
the diffuse and the saccular. Saccular aneurisms of the ascending 
or descending portion of the arch of the aorta are apt to penetrate 
the chest wall, while aneurism of the transverse aorta or diffuse 
dilatations of the whole aortic arch are more likely to extend within 
the chest without eroding the thoracic bones. Practically any 
aneurism which penetrates the thoracic bones may be inferred to 
be saccular, but if no such penetration takes place, it may be im- 
possible to make out whether the dilatation is diffuse or circum- 
scribed. I shall consider : 

I. The signs of the presence of aneurism. 

II. The evidences of its seat. 

Inspection and palpation give us most of the important informa- 
tion in the diagnosis of aneurism. The patient should be placed in 
the position shown in Fig. 117, so that the light will strike obliquely 
across the surface of the chest, and the observer should be so placed 
that his eyes are as nearly as possible at the level at that part of 
the chest at which he hopes to see pulsation. 

In the majority of cases of aneurism some abnormal pulsation 
may be made out either to the right of the sternum in front or hi 
Abnormal the region of the left scapula behind. If the aneur- 
Pulsation. i sm is large, a considerable area of the chest wall may 
be lifted with each beat of the heart ; with smaller growths the 
pulsating area may be small and sharply circumscribed. Not in- 
frequently an abnormal pulsation at the sternal notch or in the 



THORACIC ANEURISM. 



221 



neck may be observed. Other causes of abnormal pulsations in 
the chest, such as dislocation or uncovering of the heart, must of 
course be excluded. Pulsations due to aneurism can sometimes 
be distinctly seen to occur later than the apex impulse of the heart. 

Palpation controls the results of inspection, but at times a pul- 
sation may be seen better than felt ; at others may be felt better 
than seen. Bimanual palpation — one hand over the suspected area 
in front and one hi a corresponding position behind — is useful. 

If. the aneurism involves the ascending portion of the aortic 




Fig. 117.— Position When Looking for Slight Aneurismal Pulsation. 



arch, it is likely sooner or later to erode the right margin of the 
sternum and the adjacent parts of the second or third costal car- 
tilages and appear externally as a round swelling in 
which a systolic pulsation is to be seen and felt. This 
pulsation is almost always distinctly expansile in character, and 
differs in this respect from the up-and-down motion which may 
be communicated to a tumor of the chest wall by the beating of 
a normal aorta. The tumor is usually firm, rarely soft, and may 
be as hard as any variety of malignant new growth. Occasionally 



222 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



the thickness of the lamellated clot within it is so great that no 
pulsations are transmitted to the surface. 

"Whether the aneurism penetrates the chest or not, it is often 
possible to feel over it a vibrating thrill, usually sys- 
tolic in time. If the layer of lamellated clot in the 
sac is very thick, the thrill is less apt to be felt. 

More important in diagnosis is a diastolic shock or tap which is 
appreciated by laying the palm of the hand lightly over the affected 



Thrill. 




Fig. 118.— Aneurisnial Tumor (A~). The arrow B points to a gummatous swelling near the en- 
siform cartilage. The radiographic appearances of this case are shown below (Fig. 121). 



area. This diastolic shock is due to the recoil of the blood in the di- 
lated aorta, and is one of the most important and characteristic signs 
Diastolic m aneurism. As the wall of the sac becomes weaker, 
Shock, the intensity of this shock diminishes. This diastolic 
shock may be appreciated over the trachea also, and is thought by 
some to have even more significance when felt in this situation. 

Of special importance hi aneurism of the transverse arch is the 
sign known as the tracheal tug. The arch of the aorta runs over 



THORACIC ANEURISM. 



223 



the left primary bronchus in such a way that when the aorta is 
dilated, the bronchus is pressed upon with each expansile pulsation 
Tracheal °f ^ ne artery. This systolic pressure transmitted to 
Tug. the trachea produces a distinct downward tug upon it 
with each systole of the heart. The tug is best felt by making the 
patient throw back his head so as to put the trachea upon a stretch. 
The physician then stands behind him and gently presses the tips 
of the fingers of both hands up under the lower border of the cri- 




FIG. 119. 



Aneurism Tumor Perforating the Sternum at A. At B there is a gummatous 
(See below, Fig. 121, a radiograph of this case). 



coid cartilage. In feeling thus for the tracheal tug as transmitted 
to the cricoid cartilage certain precautions must be observed : 

(a) One must distinguish the tracheal tug from a simple pulsa- 
tion transmitted to the superficial tissues by the vessels under- 
neath. Such pulsation makes the tissues move out and in rather 
than up and down. 

(b) A tracheal tug felt only during inspiration has no patho- 
logical significance and is frequently present in health. 

While preparing to try for the tracheal tug we may notice 
whether there is any dislocation of the trachea, as shown by the 



224 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

displacement of Adam's apple. Other and less important signs of 
aneurism, which are due to the pressure of the dilated aorta upon 
the nerves or vessels of the mediastinum, are : 

(1) Inequality of the pupils. 

(2) Inequality of the radial pulses. 

(3) (Edema and cyanosis of one arm or of one side of the neck 
and head. 

(4) Pain in one arm from the pressure of an aneurism involving 
the subclavian artery upon the brachial plexus. 

(5) Clubbing of the fingers of one hand (rare). 

(6) Prominence of one eye (rare). 

(7) Flushing or sweating of one side of the face (very rare). 
Contraction or dilatation of the pupil is due to an irritative or 

paralytic affection of the sympathetic nerves. This symptom is 
much commoner than the other effect of pressure upon the sympa- 
thetic nerves; namely, flushing or sweating of one side of the face. 

In comparing the pulses in the two radials we must bear in mind 
the possibility of a congenital difference between them, due to a 
difference either in the size of the arteries or in their position, and 
also that a tumor pressing on the subclavian may affect the pulse 
exactly as an aneurism. The pulse wave upon the affected side 
(most often the left) may be either less in volume or later in time 
than the wave in the other radial artery, according as the pulse 
wave is actually delayed in the aneurismal sac or merely diminished 
by it. In marked cases the pulse upon the affected side may be 
nearly or quite absent. On the other hand the inequality of the 
pulses may be so slight that the sphygmograph has to be employed 
to demonstrate differences in the shape of the wave not perceptible 
to the fingers. 

Examination of the heart itself may show some dislocation of 
the organ to the left and downward, owing to the direct pressure 
of the aneurismal sac. 

II. Percussion. 

If the aneurism is deep-seated, the results of percussion are 
negative. If, on the other hand, it be situated immediately be- 



THORACIC ANEURISM. 



225 



neath the sternum or close under the thoracic wall, an area of dul- 
ness, not present in the normal chest, may be mapped out. The 
outlines most commonly seen in such cases are shown in Fig. 120. 
\Vhen the aneurism involves the descending aorta, an area of dulness 
may be found hi the region of the left scapula or below it, and pul- 
sation may be detected in the same area. 

III. Auscultation. 

The signs revealed by auscultation are not of much diagnostic 
value as a rule. In about one-half of the cases of sacculated aneu- 



Aneurismal 
dulness. ' 



Liver dulness.- - 




Heart dulness. 



Fig. 130.— Diagram of Percussion Dulness in Aortic Aneurism. 



rism there are no sounds or murmurs to be heard over the tumor. 
In other cases a systolic murmur, the audible counterpart of the 
vibratile thrill, may be heard over the area 'of pulsation, tumor, or 
dulness corresponding to the aneurismal sac. This systolic mur- 
mur may be due to many causes other than aneurism, and has noth- 
ing characteristic about it. A similar systolic sound is sometimes 
heard over the trachea (Drummond's sign) or hi the mouth, if the 
patient closes his lips around the pectoral extremity of the steth- 
oscope (Sansom's sign). 

A loud, low-pitched diastolic sound, corresponding to the pal- 
15 



226 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

pable diastolic shock, is generally to be heard in the aortic region. 
This diastolic sound, which is probably not produced by the aortic 
valves, is remarkably deep-toned and loud, and is, on the whole, the 
most important sign of aneurism revealed by auscultation. 

If a portion of either lung is directly pressed upon by the an- 
eurismal sac, we may have the signs of condensation of the lung 
in the area pressed upon (slight dulness, broncho-vesicular breath- 
ing, and exaggerated voice sounds). If one of the primary bronchi 



From the front. 



From behind. 




Fig. 121.— Radiograph of Case whose Photograph is Reproduced as Figs. 118 and 119. In the 
right-hand cut are shown the appearances seen from behind. The left-hand cut, A, A, 
aneurismal sac ; _B, heart displaced ; C, liver (not in focus). 



is pressed upon, as occasionally happens, atelectasis of the corre- 
sponding lung may be manifested by the usual signs (dulness, ab- 
sence of tactile fremitus and of respiratory and vocal sounds). 

Since aneurism is frequently associated with regurgitation at 
the aortic valve, a diastolic murmur is not infrequently to be 
heard. 

If the aneurismal sac is of very great size, the pulse wave in 
the femorals may be obliterated, as happened in a case described 
by Osier. 



THORACIC ANEURISM. 



227 



IV. Radioscopy. 

With the fluoroscope and through photography one can often 
make out a shadow corresponding to the position of the aneurism. 




Dilated aortic 
arch. 



Hypertrophied 
heart. 



Fig. 123.— Aortic Regurgitation with Diffuse Dilatation of the Aortic Arch. Front view. 



The position of the shadow is best explained by reference to Figs. 
121, 122, and 123. 

Summary. 

The most important signs of aneurism are : 

1. Abnormal pulsation — visible or palpable 

2. Tumor over which a 

3. Thrill and a 



228 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

4. Diastolic shock may be felt. 

5. Tracheal tug. 

6. Pressure signs (unequal pulses, pupils, hoarseness, pain, etc.). 

7. Dulness on percussion over the suspected area. 

8. Loud, low-pitched aortic second sound. 

9. Systolic murmur (least important of all). 




Aneurisnial sac. 



Heart displaced 
downward by 
the aneurism. 



Fig. 123.— Extensive Aortic Aneurism Displacing the Heart. 

10. Radioscopy may demonstrate a shadow higher up than that 
corresponding to the heart and extending beyond that produced by 
the sternum, spinal column, and great vessels. 

Diagnosis of the Seat of the Lesion. 

(a) Aneurism of the ascending arch generally approaches or 
penetrates the chest wall in the vicinity of the second right inter- 
costal space near the sternum. Previous to perforating the thoracic 



THORACIC ANEURISM. 229 

parietes, the growth of the aneurism may give rise to pain, pulsa- 
tion, and dulness and thrill in this region. 

(b) Aneurism of the transverse arch or diffuse dilatation of the 
aorta, such as usually occurs in long-standing cases of aortic regur- 
gitation, may not give rise to any visible pulsation of the chest 
wall, and, if deep-seated, need not produce any abnormal dulness 
on percussion. In such cases an aneurism is to be recognized, if 
at all, by evidences of pressure on the nerves or vessels of the medi- 
astinum (cough, aphonia, inequality of the pupils, tracheal tug, 
etc.). 

(c) Aneurism of the descending aorta gives rise usually to severe 
and persistent pain in the back, which radiates along the intercos- 
tal nerves or downward. Other pressure symptoms are not marked, 
but in advanced cases an area of abnormal dulness and pulsation 
may be found in the region of the left scapula or below it. 

(d) If the innominate artery or one of the carotids is involved, 
we usually find a pulsating lump in the region of one or the other 
claviculo-sternal joint or at the root of the neck, and the trachea 
may be displaced to one side. If the subclavian is involved or 
pressed upon, there may be pain and oedema in the corresponding 
arm. 

Differential Diagnosis. 

(a) Some writers draw a distinction between the diffuse dilata- 
tion of the aortic arch, which sooner or later complicates almost 
every case of incompetency of the aortic valves, and saccular aneu- 
rism of the transverse portion of the aorta. Clinically, such dis- 
tinction seems to be impossible, although if symptoms resembling 
those of aneurism gradually develop in a case of aortic regurgita- 
tion, one may suspect that the dilatation of the aorta is merely 
part of the distention of the whole arterial tree, which aortic regur- 
gitation tends to produce. 

(b) Aneurism is not infrequently mistaken for aortic stenosis, in 
which a systolic murmur and thrill, similar to those occurring in 
aneurism, are to be heard over the region of the aortic arch. From 
aortic stenosis aneurism is distinguished by the fact that it does 



230 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

not produce characteristic changes in the pulse, and by the presence 
of some one of the symptoms above described, such as tracheal 
tug, pressure symptoms, abnormal area of percussion dulness, etc. 

(c) Simple dynamic throbbing of a normal aortic arch similar 
to that which occurs in the abdominal aorta may lift the chest wall 
so as to simulate aneurism. The other positive symptoms and 
signs of aneurism are, however, absent. 

(d) Pulmonary tuberculosis or cancer of the oesophagus, produc- 
ing as they may substernal pain, cough, and aphonia by pressure 
upon mediastinal structures, have been mistaken for aneurism, 
from which, however, they may be distinguished by the absence of 
the positive signs above described, by the more rapid emaciation 
of the patient, and by the positive evidences of cancer or tubercu- 
losis. 

(e) Empyema necessitatis may produce a pulsating tumor like 
that of aneurism and the area of dulness may be similar, but there 
is no diastolic shock, no tactile thrill or murmur, and the history 
of the case is usually very different from that of aneurism. It is 
perfectly safe to insert a fine hollow needle in doubtful cases. No 
serious hemorrhage results if aneurism is present, and the diagnosis 
and treatment may be greatly assisted. 

(/) Mediastinal tumors are sometimes almost indistinguishable 
from aneurism during life. They may produce a more intense and 
widespread dulness which is usually in the median line, while the 
dulness of aneurism is oftener at one side. The pulsation transmit- 
ted to a tumor by the heart has not the expansile character of aneu- 
rismal pulsation. Tumors are not associated with any diastolic 
shock, rarely with a tracheal tug. 

The course of most mediastinal tumors is progressive and at- 
tended by great cachexia, while the symptoms of aneurism are often 
more or less intermittent, and unless pain is severe there is no such 
emaciation or ansemia as is commonly seen with mediastinal tu- 
mors. Pressure symptoms may be the same in both diseases, but 
are usually more marked with mediastinal growths. A metastatic 
nodule over the clavicle sometimes betrays the presence of a pri- 
mary focus within the chest. 






THORACIC ANEURISM. 231 

(g) Betraction of the right lung (fibroid phthisis), with or without 
displacement of the heart toward the diseased side, may uncover 
the heart so as to produce some of the signs of aneurism, i.e., pul- 
sation and dulness in the upper right intercostal spaces near the 
sternum, with a loud aortic second sound and sometimes a systolic 
murmur in the dull area.. 

The history of the case and a careful examination of the lungs 
usually suffice to set us right. 

(h) Dilatation of the heart may be so extreme that pulsation 
and percussion dulness appear in the characteristic aneurismal area 
to the right of the sternum, especially if there is solidification of 
the left lung. But the pulse is in such cases much weaker and 
more irregular than is to be expected in uncomplicated cases of aortic 
aneurism, and the history of the case is usually decisive. 



PART III. 

DISEASES OF THE LUNGS. 



CHAPTER XL 

BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 

I. Tracheitis. 

In connection with bronchitis or as a forerunner thereof, inflam- 
mation of the trachea is not uncommon. It gives rise to no char- 
acteristic physical signs, but is to be suspected when the patient 
complains of cough with pain over the upper portion of the sternum. 

Bronchitis. 

Inflammation of the larger bronchial tubes is not often the 
cause of any definite physical signs, but with every paroxysm of 
coughing the patient may feel pain in an area corresponding ex- 
actly to the anatomical position of the primary bronchi. I have 
seen patients indicate most accurately the situation of the large 
tubes when pointing out the position of pain produced by coughing. 

In the vast majority of cases of acute bronchitis the smaller 
bronchi are involved, and the swelling of their walls, with or with- 
out exudation, is manifested by the following physical signs : 1 

(1) Diminution in the intensity of vesicular breathing over the 
area affected (rarely in the earliest stages the breath sounds are 
exaggerated and harsh, especially in the upper portions of the 
chest). 

1 Bronchitis may exist without rales, but cannot be diagnosed without 
them. Occasionally they are present only in the early morning. 



234 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(2) Bales, which are squeaking or piping over bronchi which 
are narrowed without any considerable amount of exudation, as is 
the case in the earliest stages of many cases, and bubbling, crack- 
ling, or clicking in later stages, when watery or viscid exudation is 
present in the tubes. The calibre of the bronchi affected can be 
estimated from the coarseness or fineness of the rales. Low-pitched 
groaning sounds point to a stenosis of a relatively large bronchus, 
while squeaking and whistling sounds are usually produced in the 
smaller tubes. Large, bubbling rales are much less often heard 
than the finer, crackling variety. The latter are produced in the 
smallest tubes, the former in the larger variety. 

Simple non-tuberculous bronchitis is almost invariably bilateral 
or symmetrical, and affects most often the lower two-thirds of the 
lungs, leaving the apices relatively free. It is almost never con- 
fined to an apex. When rales are to be heard on one side of the 
chest only, and when they persist in the same spot for days and 
weeks, tuberculosis is always to be suspected, especially if the 
rales are localized at the summit of one or both lungs. It should 
never be forgotten that the tubercle bacillus is capable of exciting 
a bronchitis indistinguishable from other varieties of bronchitis, 
except by its tendency to show itself at the apex of the lung and 
on one side only ; most cases of pulmonary tuberculosis begin in 
this way. 

The only other variety of bronchitis which is often unilateral is 
that due to influenza bacillus. In the course of a case of influenza, 
a unilateral localized bronchitis not infrequently occurs. Over a 
patch of lung, perhaps the size of the palm of the hand, fine, moist 
rales may persist for weeks, finally clearing up only after the pa- 
tient has resumed his ordinary occupation. Doubtless such local- 
ized patches of bronchitis are often accompanied by foci of lobular 
pneumonia too small to be detected by our present methods of 
physical examination. 

Percussion dulness is absent in bronchitis except near the end 
of fatal cases, when the lung is stuffed with mucus and pus, or 
when atelectasis has occurred owing to extensive plugging of the 
larger bronchi. These events are rarely seen, and in general the 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 235 

negative results of percussion are of great value in excluding sol- 
idification or fluid exudation. 

Occasionally percussion resonance may be increased owing to 
a slight temporary overdistention of the air vesicles from coughing. 1 

Inspection usually shows little or nothing of diagnostic impor- 
tance in acute bronchitis. Long-standing cases, complicated as 
they almost invariably are by emphysema, present changes in the 
shape of the thorax ; but these are due to the emphysema rather 
than to the bronchitis. In children acute bronchitis sometimes 
involves so many of the smaller bronchi that dyspnoea and use of 
accessory muscles of respiration are' notable. But this usually 
means atelectasis, broncho-pneumonia, or laryngeal spasm, in addi- 
tion to the bronchitis. 

From violent coughing the jugulars may be distended, but no 
systolic pulsation occurs in them. 

Voice sounds and tactile fremitus are normal. 

Differential Diagnosis. 

(Edema of the lung and bronchial asthma are the only pathologi- 
cal processes (except hemorrhage into the lung substance) which 
give rise to signs like those of bronchitis. 

(1) In oedema of the lung, or pulmonary apoplexy, one may 
find, as in simple bronchitis, a diminished vesicular breathing with 
crackling rales, but oedema of the lung is almost always best marked 
in the dependent portions; that is, in the posterior parts of the 
lung if the patient has been lying upon the back, or in the lower 
lobes if he has been sitting up. The rales of oedema are always 
moist, are more uniform in size when compared to those of bron- 
chitis, and are never mingled with squeaking or groaning sounds. 
The recognition of a cause for the oedema, for example a non-com- 
pensated heart lesion, materially aids in the diagnosis. 

(2) Bronchial asthma or spasm of the finer bronchi produces dry 
squeaking and groaning sounds similar to those heard in the earlier 

1 In children examined during a crying-spell a cracked-pot sound can 
usually be elicited by percussion. This is in no way characteristic of bron- 
chitis and can often be obtained in healthy infants. 



236 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

stages of many cases of bronchitis. But in bronchial asthma the 
rales are chiefly expiratory, and expiration is prolonged and inten- 
sified. Moreover, the inhalation of a few drops of amyl nitrite will 
temporarily dispel rales due to bronchial 
spasm, while on the rales of dry bronchitis 
it has no effect (Abrams). 

(3) Broncho-pneumonia. In many 
cases of lobular or broncho-pneumonia the 
physical signs are exclusively those of the 
coexisting bronchitis. In such cases the 
diagnosis of bronchitis is not wrong, but 
does not cover the whole ground. I shall 
discuss further under broncho-pneumonia 
the evidence which leads us to suspect 
that something more than bronchitis is 
present. 

(4) Muscle sounds. Under certain 
circumstances (cold, nervousness), the 
rumbling noises produced by muscular 
contractions in the chest wall may simu- 
late rales so closely that the diagnosis of 
bronchitis may be strongly suggested. 
The differentiation between rales and 
muscle sounds has already been discussed 
(see above, p. 87). 

(5) Atelectatic crepitation. Crackling 
rales heard over the thin margins of the 
lungs at the base of the axilla or along 
the edges of the manubrium are often due 

to atelectasis (see above). From bronchitis they are distinguished 
by their situation and by the lack of symptoms. They are best 
heard at the point shown in Fig. 124. 




Fig. 124.— The Dots are Placed 
over the Area where Atelecta- 
tic Crepitation is Oftenest 
Heard. 



CI i ronic Bronch itis . 



So far as the bronchitis itself is concerned, there may be no 
difference hi the physical signs between the acute and chronic forms 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 237 

of the disease ; but in the latter one abnost invariably finds asso- 
ciated with the bronchitis itself a considerable degree of emphy- 
sema, of asthma, or of both conditions. Indeed, the foreground of 
the clinical picture and the bulk of the physical sign are made up 
by the emphysema and asthma, rather than by the bronchitis itself. 
Accordingly, I shall not discuss chronic bronchitis any further at 
this point, but will return to the subject in the chapter on Emphy- 
sema. 

CEOUPOUS PNEUMONIA. 

In its typical form croupous or fibrinous pneumonia produces 
solidification of one or more lobes, usually the lower, the process 
being accurately bounded by the interlobular fissures. Although 
the physical signs of the earlier stages differ considerably from 
those of the later ones, there seems to be no sufficient ground for 
marking off stages of engorgement and of red and gray hepatiza- 
tion, for clinically these stages cannot be distinguished. 

The solidification may begin in the deeper parts of the lung 
(" central. pneumonia"), so that no physical signs are obtainable 
until later in the course of the disease, when the process extends 
to the surface of the lung. 

Massive pneumonia, in which the bronchi as well as the air cells 
are plugged with fibrin and leucocytes, is a relatively rare form of 
the disease, but possesses great clinical importance on account of the 
marked resemblance between its physical signs and those of pleural 
effusion. 

The frequency of endocarditis and pericarditis in connection 
with lobar pneumonia, especially with those of the left side, should 
be borne in mind. 

Physical Signs. 

{a) Inspection. — The aspect of the patient frequently suggests 

the diagnosis; the face is anxious, often flushed or slightly cya- 

nosed, the flush sometimes affecting most strikingly the side of the 

face corresponding to the lung affected. 1 Herpetic vesicles ("cold 

1 Perhaps because the patient is apt to lie upon the affected side. 



238 FHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

sores ") are often to be seen around the mouth or nose. The rapid, 
difficult breathing is at once noticable, and expiration is often ac- 
companied by a grunt. The use of the accessory muscles of respi- 
ration and the dilatation of the nostrils attract attention. 

The combination of marked dyspnoea with absence of dropsy is 
met with more frequently in pneumonia than in any other disease. 
Both sides of the chest usually move alike, but occasionally the 
affected side shows deficient expansion especially in the later stages 
of the disease, and the other side of the chest shows increased re- 
spiratory movements (compensatory). Rarely the pulsations of the 
heart may be transmitted to the chest wall through the affected lung. 

When pneumonia attacks a feeble old man, or follows injuries 
(surgical pneumonia), its onset may be insidious, and none of the 
phenomena just described may be seen. 

(b) Palpation. — In the great majority of eases tactile fremitus is 
markedly increased over the affected area J but in case the bronchi 
are occluded by secretions or fibrinous exudate, fremitus may be di- 
minished or altogether absent. A few hard coughs will sometimes 
clear out the tubes and thus materially assist the diagnosis. Occa- 
sionally an increase in superficial temperature of the affected side 
may be noticed by palpation, and rarely one feels a friction rub 
due to the fibrinous pleurisy which almost invariably accompanies 
the disease. 

(c) Percussion. — Over the area affected the percussion note is gener- 
ally dull and may be almost flat, except in the earliest and latest 
stages of the disease, in which it may have a tympanitic quality with 
or without an element of slight dulness. More marked tympany is 
usually present over the unaffected lobes of the diseased lung (that 
is, over the upper lobes in the great majority of cases.) 

The conditions just described represent the great majority of 
cases, but the following exceptions occur : 

(1) In the pneumonias of children, and occasionally in adults, 
dulness may be absent. 

1 By using the edge instead of the flat of the hand the boundaries of sol- 
idified lobes may often be very accurately marked out by means of the tactile 
fremitus. 






BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 239 

(2) When the lower lobe of the left lung is affected, a distinctly 
tympanitic quality may be transmitted to the consolidated area 
from a distended stomach or colon. 

(3) In rare cases, the percussion over the consolidated area may 
be of a metallic quality, or produce the " cracked-pot " sound. 

(4) In central pneumonia there may be no change in the percus- 
sion note, or it may be unusually full and deep so that the sound 
side seems dull by comparison. 

A solidified lobe increases so much in size that the area of dul- 
ness corresponding to it often seems incredibly large. Thus, al- 
though the lower lobe reaches in health not more than half-way up 
the scapula, when solidified it produces dulness throughout nearly 
the whole back. 

The right base is the most frequent seat of pneumonic solidifica- 
tions, but the dulness corresponding to it is often first noticeable in 
the posterior axillary line. A dulness appreciable only in the front 
of the chest is almost sure to correspond to the upper lobe, while 
signs in the lower part of the right axilla correspond to the middle 
lobe. Many cases of central pneumonia first appear at the surface 
in one or the other axilla. 

As regards the amount of solidification needed to produce per- 
cussion dulness, Wintrich says that the minimum is a patch 5 cm. 
in diameter, 2 cm. deep, and superficially situated. 

Percussion often makes us aware of an increased resistance or 
diminished elasticity of the affected side, although the resistance is 
seldom as marked as in large pleural effusions. 

(d) Auscultation. — In the great majority of cases typical tubular 
breathing is to be heard over the affected area. Since a whisper 
is practically a forced expiration, this tubular quality is very well 
brought out if the patient is made to whisper "one, two, three," 
or any other succession of syllables, and by this method the fatigue 
and pain of deep breathing may be saved. By this use of the 
whispered voice one may accurately mark out the boundaries of the 
consolidated area, and demonstrate in many cases that it coincides 
with the boundaries of one lobe of the lung. 

In the earliest stages of the disease the breathing may be bron- 



240 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

cho-vesicular ; more often it is feeble or suppressed over the con- 
solidated area, and "crepitant rales," that is, very fine crackling 
sonnds, may be heard at the end of inspiration, but these are much 
more common in the stage of resolution 1 ("crepitans redux "). 

If some of the smaller bronchi are blocked, as is not infre- 
quently the case, respiration is absent or very feeble, and such 
cases are often mistaken for pleuritic effusion. In pneumonia of 
the upper lobe it is not rare for bronchial breathing to be absent 
even without plugging of the bronchi. 

In cases of "central pneumonia," that is, when the area of 
solidification is in the interior of the organ, there may be no 
change in the breath sounds, or a bronchial element may be faintly 
audible on auscultation with the unaided ear, and only by this 
method. 

The intensity of the spoken or whispered voice is greatly in- 
creased over the area of consolidation, and sometimes the words 
can be distinguished. The nasal twang known as " egopliony " is 
occasionally to be heard. In the majority of cases, as has been 
already stated, the right lower lobe posteriorly is affected, so that 
the consolidated area is immediately in apposition with the spinal 
column. Under these circumstances, it is not at all uncommon to 
hear bronchial breathing transmitted from the consolidated lobe 
to a narrow zone close along the spinal column on the sound side. 
Such a zone is often mistaken for consolidation (see Fig. 125). 

The signs are usually less marked in the axilla and in the front 
of the lung, but in a minority of cases, and especially when the 
upper lobes are affected, the signs are wholly in the front. When 
searching for evidences of consolidation in persons suspected to 
have pneumonia, one should never omit to examine the apices and 
very summit of the armpit, pressing the stethoscope up behind the 
anterior fold of the axilla. 

In examining the posterior lobes, when the patient is too weak 
to sit up and is loath even to turn upon the side, the Bowles steth- 

1 Crepitant rales are rarely heard in the pneumonias of infancy and old 
age. They are not peculiar to pneumonia, but occur in pulmonary oedema or 
hemorrhagic infarction— conditions easily distinguished from pneumonia. 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 



241 



oscope is a great convenience, owing to the ease with which its flat- 
tened extremity may be worked in between the patient and the bed- 
clothes without causing any discomfort. 

When resolution begins, the signs may suddenly and completely 
disappear within a few hours. More frequently the bronchial 
breathing is modified to broncho-vesicular, dulness and broncho- 
phony become less marked, fine crackling rales (crepitans redux) 
or coarser moist bubbles appear, and the lung gradually returns to 
its normal condition within a period of three or four days. In the 



-*" Tympany. 



Bronchial breathing 
transmitted by 
spinal column to 
sound lung. 




--Solidification. 



Fig. 125.- Diagram of Signs in Pneumonia. 



active stages of the disease the entire absence of rales is very char- 
acteristic. In about 19 per cent, of the cases the solidification of 
the lung persists after the fall of the temperature ; indeed, it may 
be weeks or even months before it clears up, and yet the lung may 
be perfectly sound hi the end. On the other hand, abscess or gan- 
grene may develop in the solidified lobe, or the latter may be trans- 
formed into a mass of tough fibrous tissue, and the adjacent portion 
of the chest may fall in (cirrhosis of the lung, chronic interstitial 
pneumonia) . 

" Wandering pneumonia " is a term applied to cases in which 
16 



242 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

the consolidation disappears in one lobe only to reappear in another, 
or spreads gradually from lobe to lobe. The physical signs in such 
cases do not differ essentially from those already described. 

Summary. 

In a typical case one finds (oftenest at the right base behind) 

1. Dulness on percussion. 

2. Increased tactile fremitus and voice sounds. 

3. Tubular breathing and occasionally crepitant rales. 

These signs occurring in connection with fever, cough, rusty 
sputa, pain in the side, dyspnoea, and herpes, are sufficient for the 
diagnosis. 

But many cases — some say the majority — are not typical when 
first seen. The following are the commonest anomalies : 

(a) There may be tympany instead of dulness, especially in 
children or when the solidification is at the'left base. 

(b) The breathing may be feeble but vesicular in character, or 
it may be absent, in case bronchi are plugged ; from the same cause 

(c) Tactile fremitus may be diminished. 

A hard cough may clear out the bronchi and produce a sudden 
metamorphosis of the physical signs with a return to the normal 
type. 

In these atypical cases, we have to fall back upon the symp- 
toms, the history, the blood, and sputa for help in the diagnosis. 

Deep-seated pneumonic processes may appear at the surface in 
out-of-the-way places, e.g. y at the summit of the axilla, and the 
area of demonstrable physical signs may be no larger than a silver 
dollar. A thorough examination of every inch of the chest is 
therefore essential in doubtful cases. 

In the later stages of the disease crepitant or other fine rales 
often appear, and the signs of solidification suddenly or gradually 
disappear. 

Differential Diagnosis. 

Pneumonic solidification is to be distinguished from 

(1) Pleuritic effusion. 

(2) Tuberculosis of the lung. 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 243 

(1) From pleuritic effusion, pneumonia is to be distinguished 
in the great majority of cases by differences in the onset, course, 
and general symptoms of the disease. In pneumonia the patient is 
far more suddenly and violently attacked, the dyspnoea is much 
greater, cough and pain are more distressing and more frequent, 
the temperature is higher, and the sputum often characteristic. In 
pleuritic effusion the dulness is usually more intense than in pneu- 
monia. Tactile fremitus and voice sounds are increased in pneu- 
monia (except when the bronchi are plugged) ; decreased or absent 
in pleuritic effusion. Bronchial breathing may be heard in both 
diseases, but is usually feeble and distant when occurring in pleu- 
risy, and loud in pneumonia. If the affection be on the left side, 
the diagnosis is much aided by the presence of dislocation of the 
heart, which is produced by pleuritic effusion and never by pneu- 
monia. In cases of pneumonia with occluded bronchi, one may 
have every sign of pleuritic effusion — flatness, absent breathing, 
voice and fremitus — and in such cases the absence of any disloca- 
tion of the heart, provided the disease is upon the left side, is very 
important. If a similar condition of things occurs upon the right 
side, one may have to fall back upon the symptoms and upon such 
evidence as the blood count, herpes, sputum, etc. 

(2) Tuberculosis of the lung causing, as it may, a diffuse sol- 
idification of the organ, may be indistinguishable from pneumonia 
if we take account only of the physical signs, but the two diseases 
can usually be distinguished without difficulty by the difference in 
their symptoms and course, and by the presence or absence of tuber- 
cle bacilli in the sputum. 

Inhalation Pneumonia. Aspiration Pneumonia. 

When food or other foreign substances are drawn into the air 
passages, as may occur, for example, during recovery from ether 
narcosis, a form of broncho-pneumonia may be set up, in which the 
solidified patches are not infrequently large enough to be recognized 
by the ordinary methods of physical examination. 

The lesions are usually bilateral and accompanied by a general 
bronchitis. Slight dulness and indistinct bronchial breathing can 



244 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

usually be made out over an irregular area in the backs of both 
lungs. 

The signs are considerably less marked than in croupous pneu- 
monia, and the boundaries of the irregular patches of disease do 
not correspond to those of a lobe of the lung. 

If not rapidly fatal, the disease may be complicated by pulmo- 
nary gangrene or abscess and large quantities of fetid pus may be 
spit up. 

Broncho-Pneumonia. 

(Catarrhal or Lobular Pneumonia.) 

Multiple small areas of solidification scattered through both 
lungs, interspersed with areas of collapse, and usually associated 
with diffuse bronchitis, occur very frequently in children producing 
severe dyspnoea, cyanosis, cough, and somnolence, and running a 
very fatal course. 

The solidified lobules may fuse so as to form considerable areas 
of hepatized lung, or there may be no lesion larger than a pea. 

This is the usual type of " lung fever " in infants, although or- 
dinary lobar pneumonia is not rare in infancy and in childhood. 

The widespread atelectasis of the lower lobes which is associated 
with the disease in most cases owing to the plugging of the bronchi 
with tenacious secretions, is probably as serious in its effects as the 
pneumonic foci themselves. 

The anterior and upper parts of the lungs often become dis- 
tended with air (vicarious emphysema) and render the physical 
signs very confusing and deceptive. 

Physical Signs. 

In the majority of cases there are no characteristic physical 
signs, and the diagnosis has to be made largely from the symptoms 
and course of the disease. The consolidated areas are usually too 
small to give rise to any dulness on percussion, or to any change in 
the breath sounds, voice sounds, or fremitus, so that auscultation 
shows, as a rule, nothing more than patches of fine rales occurring 
at the end of expiration. Localized tympanitic resonance is some- 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 245 

times present over the diseased area, making the sounder portions 
of the lungs seem dull by comparison. Occasionally, when many 
lobules have fused into a single mass of larger area, the ordinary 
signs of consolidation may be obtained, although they are apt to 
disappear within twenty-four or forty-eight hours and appear in 
another situation. As above said, the diagnosis is usually to be 
made, if at all, from the combination of the physical signs of a 
localized bronchitis with the symptoms of pneumonia. "This pa- 
tient," we say, "has only the signs of bronchitis, but he is too 
sick. The cyanosis, dyspnoea, and fever are too marked. He is 
sicker than simple bronchitis will account for. " 

Differential Diagnosis. 

(a) Acute pulmonary tuberculosis may be indistinguishable from 
broncho-pneumonia by the physical signs alone. The diagnosis 
must be made from the history and course of the disease or from 
the presence of tubercle bacilli in the sputa. 

(b) The extensive atelectasis of the lower lobes which may ac- 
company broncho -pneumonia gives rise to dulness and absence of 
respiratory and vocal sounds. Thus, the signs of pleuritic effusion 
are simulated, and in children the possibility of empyema should 
not be forgotten. As a rule, broncho-pneumonia gives rise to much 
greater dyspnoea, and is associated with a more extensive bronchitis, 
than usually coexist with pleural effusion. The atelectatic lobules 
may be expanded by coughing or by the cutaneous stimulus of cold 
water, and thus resonance and breath sounds may suddenly return. 
With pleuritic effusions, of course, such a change is impossible. 

TUBEKCULOSIS OF THE LUNGS. 

(1) Incipient Tuberculosis. 

In the earlier stages of the disease there may be absolutely no 
recognizable physical signs, and the diagnosis may be established 
only by the positive result of a tuberculin injection or by the com- 
bination of debility with slight fever not otherwise to be accounted 
for. 



246 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

In some cases the earliest evidence of the disease is hcemoptysis. 1 
When a patient consults a physician on account of haemoptysis, it 
is frequently impossible to find any physical signs of disease in the 
lungs ; not until weeks or months later do the characteristic changes 
recognizable by physical examination make their appearance. 

The very early hoarseness of the voice in tuberculous patients is 
of great importance and often attracts Our attention to the lungs 
when the patient has said nothing about them. Definite physical 
signs in the lungs and tubercle bacilli in the sputa (artificially ob- 

Rales. _ 




Fig. 126.— Diagram to Show Position of Earliest Signs in Tuberculosis. 



tained through the use of potassic iodide, see below) may occasion- 
ally be demonstrated before any cough has appeared. On the other 
hand, the patient may cough for weeks before anything abnormal 
can be discovered in the lungs. Occasionally tuberculosis begins 
with an ordinarily bilateral bronchitis. I have found tubercle ba- 
cilli in four such cases. More often the earliest physical signs 
are: 

(a) Fine crackling rales at the apex of one lung, heard only 

1 Never percuss a patient within forty-eight hours after a hemorrhage, and 
never encourage cough or forced respiration in such a one. There is danger 
of starting a fresh hemorrhage. 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 247 

with or after cough and at the end of inspiration. [More rarely 
squeaks may be heard.] (See Fig. 126). 

(b) A slight diminution in the excursion of the diaphragm on 
the affected side, as shown by Litten's diaphragm shadow. 

(c) Slight diminution in the intensity of the respiratory mur- 
mur, with or without interrupted inspiration ("cog-wheel breath- 
ing"). 

(a) In examining the apices of the lungs for evidence of early 
tuberculosis one should secure if possible perfect quiet in the room, 
and have the clothes entirely removed from the patient's chest. 
The ordinary hard-rubber chest-piece is better than the chest-piece 
of the Bowles instrument when we wish to search the apices for 
fine rales. After listening during quiet breathing over the apices 
above and below the clavicle in front, and above the spine of 
the scapula behind, the patient should be directed to breathe out 
and then, at the end of expiration, to cough. During the deep 
inspiration which is likely to precede or to follow such a cough one 
should listen as carefully as possible at the apex of the lung, above 
and below the clavicle, concentrating attention especially upon the 
last quarter of the inspiration, when rales are most apt to appear. 
Sometimes only one or two crackles may be heard with each inspi- 
ration, and not infrequently they will not be heard at all unless the 
patient is made to cough, but even a single rale, if persistent, 1 is 
important. In children who cannot cough at will, one can accom- 
plish nearly the same result by making them count as long as pos- 
sible with one breath and then listening to the immediately suc- 
ceeding inspiration. When listening over the apex of the lung, 
one should never allow the patient to turn his head sharply in the 
other direction, since such an attitude stretches the skin and mus- 
cles on the side on which we are listening so as to produce annoy- 
ing muscle sounds or skin rubs. 

In cases in which one suspects that incipient tuberculosis is 

1 Rales heard only during the first few breaths and not found to persist on 
subsequent examinations, may be due to the expansion of atelectatic lobules 
(see above, p. 105) . 



248 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

present and yet in which no positive evidence can be found, it is a 
good plan to give iodide of potassium (gr. vii. three times a day) for 
a few days. The effect of this drug is often to make rales more 
distinct, and sometimes to increase expectoration so that tubercle 
bacilli can be demonstrated when before none were to be obtained. 1 

(b) The diminution in the excursion of the diaphragm upon the 
affected side in cases of incipient phthisis has been much insisted 
upon by F. H. Williams and others who have interested themselves 
in the radioscopy of the chest. Litten's diaphragm shadow gives 
us a method of observing the same phenomenon without the need 
of a fluoroscope. Even very slight tuberculous changes in the lung 
are sufficient to diminish its elasticity and so to restrict its excur- 
sion and that of the diaphragm. Comparisons must always be 
made with the sound side in such cases, as individuals differ very 
much in the extent with which they are capable of depressing the 
diaphragm. It must be remembered that pleuritic adhesions, due 
to a previous inflammation of the pleura, may diminish or alto- 
gether abolish the excursion of the diaphragm shadow, independ- 
ently of any active disease in the lung itself. 

Those who are expert in the use of the fluoroscope believe that 
they can detect the presence of tuberculosis in the lung by radi- 
oscopy at a period at which no other method of physical examina- 
tion shows anything abnormal. I shall return to the consideration 
of this point in the section on Kadioscopy. 2 

Interrupted or cog-wheel respiration, in which the inspiration 
is made up of sharp, jerky puffs, signifies that the entrance of the 
air into the alveoli is impeded, and such impediment is most likely 
to be due to tuberculosis when present over a considerable period 
in a localized area of pulmonary tissue. 

1 Any irritating vapor — for example, creosote vapor — which produces vio- 
lent cough and expectoration, may be used to expel bronchial secretions in 
doubtful cases. Tubercle bacilli may then be found in the sputum of patients 
who, without the irritating inhalation, have no cough and so no sputa. 

2 See Appendix C. 



BRONCHITIS, PNEUMONIA. TUBERCULOSIS. 



249 



(2) Moderately Advanced Cases 

So far I have been speaking of the detection of tuberculosis at 
a stage prior to the production of any considerable amount of solid- 
ification. The signs considered have been those of bronchitis 
localized at the apex of the lung, or of a slightly diminished pul- 
monary elasticity, whether due to pleuritic adhesions or to other 
causes. We have next to consider the signs in cases in which so- 
lidification is present, though relatively slight in amount. This 
condition is comparatively easy to recognize when it occurs at the 



Rales. ->_ 




.^ Complete 
. solidification. 



Partial 
solidification. 



_ —\~~ Rales. 



Fig. 127.— Diagram of Signs in Phthisis. 



left apex, but more difficult in case only the right apex is diseased. 
Partial solidification of a small area of lung tissue at the left apex 
gives rise to 

(a) Slight dulness on light percussion, 1 with increased resist- 
ance. 

(b) Slight increase in the intensity of the spoken and whispered 
voice, and of the tactile fremitus (hi many cases) 

1 Other causes of dulness, such as asymmetry of the chest, pleural thicken- 
ing, and tumors, must be excluded. Emphysema of the lobules surrounding 
the tuberculous patch may completely mask the dulness. 



250 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST 

(c) Some one of the numerous varieties of broncho-vesicular 
breathing (true bronchial breathing is a late sign). 

(d) Abnormally loud transmission of the heart sounds, espe- 
cially under the clavicle. 

(e) Cardiorespiratory murmurs (vide p. 139) are occasionally 
due to the pressure of a tuberculous lobule upon the subclavian 
artery. In connection with other signs they are not altogether 
valueless in diagnosis. 

In case there is also a certain amount of secretion in the bron- 
chi of the affected area or ulceration around them, one often hears 
rales of a peculiar quality to which Skoda has given the name of 
" consonating rales." Kales produced in or very near a solidified 
area are apt to have a very sharp, crackling quality, their intensity 
being increased by the same acoustical conditions which increase 
the intensity of the voice sounds over the same area. When such 
rales are present at the apex of either lung, the diagnosis of tuber- 
culosis is almost certain, but if, as not infrequently occurs, there 
are no rales to be heard over the suspected area, our diagnosis is 
clear only in case the signs occur at the left apex. Precisely the 
same signs, if present at the right apex, leave us in doubt regard- 
ing the diagnosis, for the reason that, as has been explained above, 
we find at the apex of the right lung in health signs almost exactly 
identical with those of a slight degree of solidification. Hence, if 
these signs, and only these, are discovered at the right apex, we 
cannot feel sure about the diagnosis until it is confirmed by the 
appearance of rales in the same area of the left side (whether under 
the influence of iodide of potassium or spontaneously), or by the find- 
ing of tubercle bacilli in the sputum. 1 

A sign characteristic of early tuberculous changes in the lung and 
one which I have frequently observed in the lower and relatively 
sounder lobes of tuberculous lungs is a raising of the pitch of inspi- 
ration, without any other change in the quality of the breathing or 
any other physical signs. The importance of this sign in the diag- 

1 The natural disparity between the two apices is less marked in the supra- 
spinous fossa behind than over the clavicle in front, and hence pathological 
dulness at the apex is more often demonstrable behind than in front. 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 



251 



nosis of early tuberculosis of the lungs was insisted upon by the 
elder Flint in his work on "The Respiratory Organs " (1866), and 
has more recently been mentioned by Norman Bridge. 

It must never be forgotten that tuberculosis may take root in 




Fig. 128 —This Patient has Solidification at both Apices and Tubercle Bacilli in the Sputa. 

feels perfectly well. 



He 



the most finely formed chests and in persons apparently in blooming 
health. The "phthisical chest " and the sallow, emaciated figure of 
the classical descriptions apply only to very advanced cases. Fig. 
128 represents a patient with moderately advanced signs of phthisis 
and abundant tubercle bacilli in the sputa. He feels perfectly 



252 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

well and is at work. On the other hand, a patient with very slight 
signs may be utterly prostrated by the toxaemia of the disease. 

(3) Advanced Phthisis. 

Characteristic of the more advanced stages of tuberculosis in the 
lungs is the existence of large areas of solidified and retracted lung, 
and, to a lesser extent, the signs of cavity formation. The patients 
are pale, emaciated, and feverish. The signs of solidification have 
already been enumerated in speaking of pneumonia. They are : 

1. Marked dulness, or even flatness, 1 with increased sense of re- 
sistance. 

2. Great increase of voice sounds or of tactile fremitus. 

3. Tubular breathing, sometimes loud, sometimes feeble. 

4. As a rule, coarse rales, due to breaking down of the caseous 
tissue, are also to be heard over the solidified areas. Sometimes 
these rales are produced within the pleuritic adhesions, which are 
almost invariably present in such cases. If they disappear just 
after profuse expectoration, one may infer that they are produced 
within the lung. 

Increase in the intensity of the spoken voice, of the whispered 
voice, or of the tactile fremitus may be marked and yet no tubular 
breathing be audible. Each of these signs may exist and be of im- 
portance as signs of solidification without the others. As a rule, 
it is true, they are associated and form a very characteristic group, 
but there are many exceptions to this rule. 

The tendency of the spinal column to transmit to the sound 
lung sounds produced in an area of solidification immediately 
adjacent to it on the other side, has been already alluded to in 
the section on pneumonia, and what was then said holds good of tu- 
berculous solidification. Owing to this it is easy to be misled into 
diagnosing solidification at both apices when only one is affected. 

Since solidification is usually accompanied by retraction in the 
affected lung in very advanced cases, the chest falls in to a greater 

1 Unless senile emphysema masks it. Fibroid phthisis {vide infra) may 
show no dulness. Remember that gastric tympany may be transmitted to the 
left lung and mask dulness there. 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 



253 



or less extent over the affected area, and the respiratory excursion 
is much diminished, as shown by ordinary inspection and by the 
diminution or disappearance of the excursion of the diaphragm 
shadow. The intensity of the tubular breathing depends on the 
proximity of the solidified portions to the chest wall and to the 
large bronchi, as well as on the presence or absence of pleuritic 
thickening. 

It is rare to find a whole lung solidified. The process, begin- 
ning at the apex or just below, extends down as far as the fourth 



Bronchial breath- 
ing, dulness. 

Increased fremitus. 

Increased voice 
sounds. 




Fig. 129.— To Illustrate Progress of Signs in Pulmonary Tuberculosis. 



rib in front, i.e., through the upper lobe, in a relatively short time, 
but below that point its progress is comparatively slow and the 
lower lobes may be but little affected up to the time of death. On 
the relatively sound side the exaggerated (compensatory) resonance 
may mask the dulness of a beginning solidification there, which 
sooner or later is almost sure to occur. It is exceedingly rare for 
the disease to extend far in one lung without involving the other. 

About the time that the tuberculous process invades the previ- 
ously sound lung it is apt to show itself at the apex of the lower lobe 



254 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

of the lung first affected. Consonating rales appear posteriorly along 
the line which the vertebral border of the scapula makes when the 
arm is raised over the shoulder. These points are illustrated in 
Fig. 129. 

Cavity Formation. 

Cavities of greater or lesser extent are formed in almost every 
case of advanced phthisis, but very seldom do they attain such size 
as to be recognizable during life. Indeed, the diagnosis of cavity 
in phthisis plays a much larger part in the text-books than it does 
in the practice of medicine, since to be recognizable by physical 
examination a~ cavity must not only be of considerable size but its 
walls must be rigid and not subject to collapse, 1 it must communi- 
cate directly with the bronchus and be situated near the surface of 
the lung, and it must not be filled up with secretions. It can read- 
ily be appreciated that it is but seldom that all these conditions are 
present at once ; even then the diagnosis of cavity is a difficult one, 
and I have often known skilled observers to be mistaken on this 
point. 

The signs upon which most reliance is usually placed are : 

(a) Amphoric or cavernous breathing. 

(b) " Cracked-pot resonance " on percussion. 

(c) Coarse, gurgling rales. 

(a) Cavernous or Amphoric Respiration. — When present, this 
type of breathing is almost pathognomonic of a cavity. It is also 
to be heard in pneumothorax, but the latter disease can usually 
be distinguished by the associated physical signs. Cavernous 
breathing differs from bronchial or tubular breathing in that its 
pitch is lower and its quality hollow. The pitch of expiration 
is even lower than that of inspiration. Since a pulmonary cavity 
is almost always surrounded by a layer of solidified lung tissue, we 
usually hear around the area occupied by the cavity a ring of bron- 
chial breathing with which we can compare the quality of the cav- 
ernous sounds. 



1 Yet not so rigid as to be uninfluenced by the entrance and exit of air. 






BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 255 

(b) Percussion sometimes enables us to demonstrate a circum- 
scribed area of tympanitic resonance surrounded by marked dul- 
ness. More often the "cracked-pot" resonance can be elicited by 
percussing over the suspected area while the chest-piece of the 
stethoscope is held close to the patient's open mouth. 

Cracked-pot resonance is often absent over cavities ; rarely oc- 
curs in any other condition {e.g., in percussing the chest of a 
healthy, crying baby, and occasionally over solidified lung). 

(c) The voice sounds sometimes have a peculiar hollow quality 
(amphoric voice and whisper). 

(d) Cough or the movements of respiration may bring out over 
the suspected area splashing or gurgling sounds, or occasionally 
a metallic tinkle. Flint has also observed a circumscribed bulging 
of an interspace during cough. Bruce noted a high-pitched suck- 
ing sound during the inspiration following a hard cough ("rubber- 
ball sound"). 

Very important in the diagnosis of cavity is the intermitte7ice of 
all above-mentioned signs, which are present only when the cavity 
is comparatively empty, and disappear when it becomes wholly or 
mostly filled with secretions. For this reason, the signs are very 
apt to be absent in the early morning before the patient has expelled 
the accumulated secretions by coughing. 

Wintrich noticed that the note obtained when percussing over 
a pulmonary cavity may change its pitch if the patient opens his 
mouth. Gerhardt observed that the note obtained over a pulmo- 
nary cavity changes if the patient shifts from an upright to a re- 
cumbent position. Neither of these points, however, is of much 
importance in diagnosis. The same is true of metamorphosing 
breathing (see above, p. 98). 

Tuberculous cavities differ from those produced by pulmonary 
abscess or gangrene in that the latter are usually situated in the 
lower two-thirds of the lung. Bronchiectasis, an exceedingly rare 
condition, cannot be distinguished by physical signs alone from a 
tuberculous cavity. 



256 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Fibro id Fh th is is . 

This term applies to slow tuberculous processes with relatively 
little ulceration and much fibrous thickening. 

In a considerable number of cases the physical signs do not 
differ materially from those of the ordinary ulcerating forms of 
the disease, but occasionally when a slow chronic process at the 
apex of the lung results in the falling-away of the parenchyma of 
the lung so that we have left a cluster of bronchi matted together 
by fibrous tissue, the percussion note may be noticeably tympani- 
tic; similar tympany may be due to emphysema of the lobules 
surrounding the diseased portion. In such cases rales are usu- 
ally entirely absent ; otherwise, the signs do not differ from those 
of ordinary phthisis, except that falling-in of the chest walls over 
the retracted lung may be more marked. Occasionally the heart 
maybe drawn toward the affected lobes, e.g., upward and to the 
right in right-sided phthisis at the apex. In two cases of fibroid 
disease at the left base, Flint found the heart beating near the 
lower angle of the left scapula. 

Phthisis with Predominant Pleural Thickening. 

Tuberculosis in the lung is in certain cases overshadowed by the 
manifestations of the same disease in the pleura, so that the signs 
are chiefly those of thickened pleura. To this subject I shall return 
in the section of Diseases on the Pleura (see below, p. 271). 

Emphysematous Form of Phthisis. 

Tubercle bacilli are not very infrequently found in the sputa of 
cases in which the history and physical signs point to chronic bron- 
chitis with emphysema. I have seen two such cases within a year 
Dulness is wholly masked by emphysema, tubular breathing is 
absent, and piping and babbling rales are scattered throughout both 
lungs. The emphysema may be of the senile or small-lunged type, 
as in one of my recent cases (with autopsy), or it may be associ- 
ated with huge downy lungs and the "barrel chest." Such cases 



BRONCHITIS, PNEUMONIA, TUBERCULOSIS. 257 

cannot be identified as phthisis during life unless we make it an 
invariable rule to examine for tubercle bacilli the sputa of every 
case in which sputa can be obtained, no matter what are the physi- 
cal signs. 

Phthisis icith Anomalous Distribution of the Lesions. 

Very rarely a tuberculous process may begin at the base of the 
lung When the process seems to begin in this way, a healed focus 
is often to be found at one apex surrounded by a shell of healthy 
lung. 

The summit of the axilla should always be carefully examined, 
as tuberculous foci may be so situated as to produce signs only at 
that point. 

Another point often overlooked in physical examination is the 
lingula pulmonalis or tongue-like projection from the anterior mar- 
' gin of the left lung overlapping the heart. Tuberculosis is some- 
times found further advanced at this point than anywhere else. 

As a rule cases in which signs like those of phthisis are found 
at the base of the lung turn out to be either empyema, or abscess, 
or unresolved pneumonia (cirrhosis of the lung). 

Acute Pulmonary Tuberculosis. 

No one of the three forms in which acute phthisis occurs, viz., 

(a) Acute tuberculous pneumonia, 

(b) Acute tuberculous bronchitis and peribronchitis, 

(c) Acute miliary tuberculosis, involving the lungs, can be rec- 
ognized by physical examination of the chest. The first form is 
almost invariably mistaken for ordinary croupous pneumonia, until 
the examination of the sputa establishes the correct diagnosis. In 
the other two forms of the disease, the physical signs are simply 
those of general bronchitis. 

17 



CHAPTER XII. 

EMPHYSEMA, ASTHMA, 'PULMONARY SYPHILIS, ETC. 

I. Emphysema. 

For clinical purposes, the great majority of cases of eniphy- 
senia may be divided into two groups. 

(1) Large-lunged emphysema, usually associated with chronic 
bronchitis and asthma. 

(2) Small-lunged, or senile, emphysema. 

Although the second of these forms is exceedingly common, it 
is so much less likely than the first form to give rise to distressing 
symptoms that it is chiefly the large -lunged emphysema which is 
seen by the physician. In both conditions Ave have a dilatation 
and finally a breaking down of the alveolar walls until the air spaces 
are become relatively large and inelastic. In both forms, the elas- 
ticity of the lung is diminished ; but in the large -lunged form we 
have an increase in the volume of the whole organ in addition to 
the changes just mentioned. 

Large-Lunged Emphysema. 

The diagnosis can usually be made by inspection alone. In 
typical cases the antero-posterior diameter of the chest is greatly 
increased, the in-spaces are widened, and the costal angle is blunted, 
while the angle of Ludwig 1 becomes prominent. The shoulders are 
high and stooping and the neck is short (see Eig. 130). The patient 
is often considerably cyanosed, and his breathing rapid and difficult. 
Inspiration is short and harsh ; expiration prolonged and difficult. 
The ribs move but little, and, owing to the ossification of their car- 

1 Formed by the junction of the manubrium with the second piece of the 
.sternum. 



EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 259 



tilages, are apt to rise and fall as if made in one piece (en cui- 
rasse). The working of the auxiliary muscles of respiration is not 
infrequently seen. The diaphragm shadow (Litten's sign) begins 
its excursion one or two ribs farther down than usual and moves a 
much shorter distance than in normal cases. 

Palpation shows a diminution in the tactile fremitus, through- 
out the affected portions ; that is, usually throughout the whole of 
both lungs. Sometimes it is 
scarcely to be perceived at all. 

Percussion yields very in- 
teresting information. The 
disease manifests itself — 

(a) By hyper-resonance on 
percussion, with a shade of 
tympanitic quality in the note. 

(b) By the extension of the 
margins of the lung so that 
they encroach upon portions of 
the chest not ordinarily reso- 
nant. 

The degree of hyper-reso- 
nance depends not only upon 
the degree of emphysema but 
upon the thickness of the chest 

walls. The note is most resonant and has most of the tympanitic 
quality when the disease occurs in old persons with relatively thin 
chest walls. The encroachment of the over-voluminous lungs upon 
the liver and heart is demonstrated by the lowering of the line of 
liver flatness from its ordinary position at the sixth rib to a point 
one or two interspaces farther down or even to the costal margin, 
while the area of cardiac dulness may be altogether obliterated, 
the lungs completely closing over the surface of the heart. At the 
apices of the lungs resonance may be obtained one or two centi- 
metres higher than normally and the quality may be markedly tym- 
panitic. In the axillae and in the back the pulmonary resonance 
extends down one inch or more below its normal position. 




Fig. 130.— Barrel Chest due to Chronic Bron- 
chitis and Emphysema. 



260 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Auscultation shows in uncomplicated cases no very marked mod- 
ification of the inspiratory murmur, which, however, may be short- 
ened and enfeebled. The most striking change is a great prolonga- 
tion and emfeeblement of expiration, with a lowering of its pitch 
(see Fig. 131). 

This type of breathing is like bronchial breathing in one re- 
spect ; namely, that in both of them expiration is made prolonged, 
but emphysematous breathing is feeble and low- 
pitched, while bronchial breathing is intense 
and high-pitched. At the bases of the lungs 
the respiration is especially feeble and may be 
altogether replaced by crackling rales. 

In " small-lunged emphysema " we have 
precisely the same physical signs, except that 
illustrate ^mphyse- the boundaries of the lung are not extended, 
matous Breathing expiration is less prolonged and less difficult, 

with Musical Expira- \ . . . _ Tl , , . ' 

tory Rales. and inspiration is normal. It does not tend 

to be complicated by bronchitis and asthma; 
indeed the small-lunged emphysema rarely gives rise to any symp- 
toms, and is discovered as a matter of routine physical examination. 

Summary. 

1. Hyper-resonance on percussion. 

2. Feeble breathing with prolonged expiration. 

3. Diminished fremitus and voice sounds. 

4. Encroachment of the resonant lungs on the heart and liver 
dulness (in the large-lunged form). 

Differential Diagnosis. 

(a) Emphysema may be confounded with pneumothorax, since in 
both conditions hyper-resonance and feeble breathing are present. 
But emphysema is usually bilateral, encroaches upon but does not 
displace neighboring organs, and is not often associated with hydro- 
thorax. Emphysema, if extensive, is usually associated with 
chronic bronchitis and so with squeaking or bubbling rales, while in 



EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 261 

pneumothorax breathing is absent or distant amphoric without 
rales. 

(b) The signs of aneurism of the aorta pressing on the trachea 
or on a primary bronchus are sometimes overlooked because the fore- 
ground of the clinical picture is occupied by the signs of a coexist- 
ing bronchitis with emphysema. The cough and wheezing which 
the presence of the aneurism produces may then be accounted for 
as part of the long-standing bronchitis, and the dulness and thrill 
over the upper sternum to which the aneurism naturally gives rise 
may be masked by extension of lung borders. But the evidence of 
pressure on mediastinal nerves and vessels (aphonic, unequal pulses 
or pupils, etc.), and the presence of a diastolic shock and tracheal 
tug are usually demonstrable ; the danger is that we shall forget to 
look for them. 

(c) Uncompensated mitral stenosis may produce dyspnoea and 
cyanosis and weak rapid heart action somewhat similar to that seen 
in emphysema, and may not be associated with any cardiac mur- 
mur, but the dyspnoea is not of the expiratory type, and the irregu- 
larity of the heart, with evidence of dropsy and general venous 
stasis, should make it evident that something more than simple em 
physema is present. 

(d) The occurrence of an emphysematous form of phthisis I 
have already mentioned in discussing the latter disease (see p. 256). 

Emphysema ivith Bronchitis or Asthma. 

In the great majority of cases, emphysema of the lungs is asso- 
ciated with chronic bronchitis and very often with asthmatic parox- 
ysms. Such association is especially frequent in elderly men who 
have had a winter cough for many years and in whom arterio-scle- 
rosis is more or less well marked. In such cases the prolonged and 
feeble expiration is usually accompanied by squeaking and groaning 
sounds, or by moist rales of various sizes and in various parts of 
the chest. When the asthmatic element predominates, dry rales 
are more noticeable, and occur chiefly or wholly during expiration, 
while inspiration is reduced to a short, quick gasp. 



262 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Interstitial Emphysema. 

In rare cases violent paroxysms of coughing may rupture the 
walls of the alveoli so as to allow the passage of air into the inter- 
stitial tissue of the lung, from whence it may work through and 
manifest itself under the skin, giving rise to a peculiar crackling 
sensation on palpation, and to a similar sound on auscultation. 
More frequently the trouble arises in connection with a tracheot- 
omy wound, the air penetrating under the skin and producing a 
downy, crepitating swelling. 

" Complementary Emphysema" 

When extra work is thrown upon one lung by loss of the func- 
tion of the other, as in pleuritic effusion — a true hypertrophy of the 
overworked sound lung may take place. The elasticity of the lung 
is not diminished as in emphysema, but is greatly increased. 
Hence the term coniplenientary emphysema should be dropped and 
the term complementary (or compensatory) hypertrophy substituted. 

Like emphysema, this condition leads to hyper-resonance on per- 
cussion and to encroachment of the pulmonary margins upon the 
neighboring organs (as shown by a reduction in the area of dulness 
corresponding to them), but the respiratory murmur is exaggerated 
and has none of the characteristics of emphysematous breathing. 

A word may here be added regarding the condition described 
by West under the name of 

Acute Pulmonary Tympanites. 

In fevers and other acute debilitating conditions West has ob- 
served that the lungs may become hyper-resonant and somewhat 
tympanitic on percussion, owing, he believes, to a loss of pulmo- 
nary elasticity. The tympanitic note, often observable around the 
solidified tissue in pneumonia, is to be accounted for, he believes, 
in the same way. Like the shortening of the first heart sound, i 
acute pulmonary tympanites points to the weakening of muscle fibre 
which toxaemia is so apt to produce. Apparently the muscle fibres 
of the lung suffer like those of the heart. 



EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 263 

BKONCHIAL ASTHMA. 

(Primary Spasm of the Bronchi). 

During a paroxysm of bronchial asthma our attention is at- 
tracted even at a distance by the loud, wheezing, prolonged expira- 
tion preceded by an abortive gasping inspiration. The breathing 
is labored, much quickened in rate, and cyanosis is very marked. 
The chest is distended and hyper-resonant, the position of the dia- 
phragm low and its excursion much limited, and the cardiac and 
hepatic dulness obliterated by the resonance of the distended lungs. 
On auscultation, practically no respiratory murmur is to be heard 
despite the violent plunging of the chest walls. We hear squeaks, 
groans, muscular rumbles, and a variety of strange sounds, but 
amid them all practically nothing is to be heard of the breath 
sounds. "The asthmatic storm flits about the chest, now here now 
there," the rales appearing and disappearing. 

At the extreme base of the lungs there may be dulness due to 
atelectasis of the thin pulmonary margins. 

Differential Diagnosis. 

(a) Mechanical irritation of the bronchi, as by the pressure of 
an aneurism or enlarged gland, may set up a spasm of the neigh- 
boring bronchioles much resembling that of primary bronchial 
asthma, but thorough examination should reveal other evidence 
of mediastinal pressure, and the history of the case is very different 
from that of asthma. 

(b) Spasm of the glottis produces a noisy dyspnoea, but the diffi- 
culty is with inspiration, instead of with expiration, and the crow- 
ing or barking sound is not like the long wheeze of asthma. No 
rales are to be heard, and the signs in the lungs are those of col- 
lapse instead of the distention characteristic of asthma. 

(c) The paroxysmal attacks of dyspnoea, which often occur in 
chronic nephritis, myocarditis, and other diseases of the heart and 
kidney, may be entirely indistinguishable from primary bronchial 
asthma but for the evidence of the underlying cardiac or renal dis- 



264 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

ease. As a rule, however, the element of spasm is much less 
marked ; the breathing is quick and labored but not wheezing, expi- 
ration is less prolonged, and the squeaking and groaning rales of 
asthma are not present. 

SYPHILIS OF THE LUNG. 

The diagnosis cannot be made with certainty from the physical 
signs, and rests entirely (in the rare cases in which it is made at all) 
on the history, the evidence of syphilis elsewhere in the body, and 
the result of treatment. Most cases are mistaken for phthisis. 

Any case supposed to be phthisis, but in which the examination 
of the sputa for tubercle bacilli is repeatedly negative, should be 
given a course of syphilitic treatment. 

The physical signs, as in phthisis, are those of localized bron- 
chitis or of solidification, but the lesions are not at the apex but 
usually about the root of the lung or lower down. Cavities are not 
formed. Stenosis of a bronchus may occur with resulting atelecta- 
sis of the corresponding lobules. 

Bronchiectasis (Bronchial Dilatation). 

This rare disease is still more rarely to be recognized during 
life. It is suggested by the history of raising within a few seconds 
or minutes a very large amount of sputa, a pint or more in marked 
cases. The physical signs may not be in any way distinctive, or 
may be those of pulmonary cavity due to tuberculosis. From the 
latter bronchiectasis is to be distinguished in some cases by a 
knowledge of the previous history. Signs of cavity in phthisis are 
preceded and surrounded by signs of solidification in the same area, 
while in bronchiectasis this is not the case. Again, a bronchiecta- 
tic cavity is apt to occur, not at the apex, as in phthisis, but in the 
middle and lower thirds of the lung posteriorly. Aside from the 
history and situation of the cavity arid the presence or absence of 
solidification around it, we cannot tell from physical signs whether 
it be due to tuberculosis or to dilatation of a bronchus. In either 
case we have the signs discussed on page 254 (cracked-pot reso- 



EMPHYSEMA, ASTHMA, PULMONARY SYPHILIS, ETC. 265 

nance, amphoric breathing and voice sounds, coarse gurgling or 
splashing sounds on cough) — all these signs disappearing when the 
cavity becomes filled with secretions. 

The disease may cause marked retraction of the chest on the 
affected side, and neighboring organs may be drawn out of place. 

Cirrhosis of the Lung. 

(Chronic Interstitial Pneumonia.) 

As an end stage of unresolved croupous pneumonia, or as a 
result of chronic irritation from mineral or vegetable dust, a shrink- 
age of a part or the whole of the lung may occur, which progresses 
until the pulmonary tissue is transformed into a 'fibrous mass en- 
closing bronchi. 

The side of the chest corresponding to the affected lung becomes 
shrunken and concave ; fremitus is increased, percussion resonance 
diminished or lost, respiration tubular with coarse rales. 

From tuberculosis the condition is to be distinguished solely by 
the history, the absence of bacilli in the sputa, and the comparative 
mildness of the constitutional symptoms. 

The right ventricle of the heart may become hypertrophied and 
later dilated with resulting tricuspid insufficiency. 



CHAPTER XIII. 

DISEASES AFFECTING THE PLEUKAL CAVITY. 

I. Hvdrothorax. 

In cases of nephritis or of cardiac weakness due to valvular 
heart disease a considerable accumulation of serum may take place 
in both pleural cavities. The physical signs are identical with 
those of pleuritic effusion (see below, page 273) except that the 
latter is almost always unilateral, while hydrothorax is usually bi- 
lateral. Exceptions to this rule occur, however, especially on the 
right side or in cases in which one pleural cavity has been obliter- 
ated by fibrous adhesions, the results of an earlier pleurisy. The 
fluid obtained by tapping in cases of hydrothorax is usually con- 
siderably lower in specific gravity and poorer in albumin than that 
exuded in pleuritic inflammation. 

The fluid shifts more readily with change of position than is the 
case with many pleuritic effusions, owing to the absence of adhe- 
sions in hydrothorax. 

Friction sounds, of course, do not occur, as the pleural surfaces 
are not inflamed. A few grains of potassium iodide by mouth soon 
produce a reaction for iodine in the fluid of hydrothorax and not in 
pleuritic effusion. 

II Pneumothorax. 

Pneumothorax, or the presence of air in the pleural cavity, may 
result from stabs or wounds of the chest wall, but is usually a com- 
plication of pulmonary tuberculosis which weakens the lung until 
by a slight cough or even by the movements of ordinary respiration 
the pulmonary pleura is ruptured and air from within the lung leaks 
into the pleural cavity. 

If the opening is of considerable size, and the air is not hindered 



DISEASES AFFECTING THE PLEURAL CAVITY. 267 

or encapsulated by adhesions, great and sudden dyspnoea with pain 
and profound " shock " may result. More commonly the air enters 
the pleural cavity gradually, the other lung has time to hyper- 
trophy, and the heart and other organs become gradually accus- 
tomed to their new situations. 

Physical Signs. 

1. Inspection. — The affected side may lag behind considerably in 
the movements of respiration. In very marked cases it is almost 
motionless and the interspaces are more or less obliterated. The 
diaphragm is much depressed and Litten's sign absent. In right- 
sided pneumothorax, which is relatively rare, the liver is depressed 
and the edge can be felt below the ribs. 

The heart is displaced as by pleuritic effusion, but usually to a 
less extent. With left-sided pneumothorax the cardiac impulse 
may be lowered as well as displaced, owing to the descent of the 
diaphragm. 

2. Palpation. — Fremitus is absent over the lower portions of the 
chest corresponding to the effused air. At the summit of the chest 
over the retracted lung, fremitus may be normal or increased. In 
rare cases when the lung is adherent to the chest wall and cannot 
retract, fremitus is preserved. 

The positions of the heart and liver are among the most impor- 
tant points determined by palpation. Not infrequently no cardiac 
impulse is to be obtained. Sometimes it may be felt to the right 
of the sternum (see Fig. 132) or in the left axilla, but not infre- 
quently it is so fixed by pleuropericardial adhesions that it is drawn 
upward toward the retracted lung or remains near its normal situa- 
tion. The liver is greatly depressed in cases of right-sided pneumo- 
thorax, and may be felt as low as the navel. 

3. Percussion. — Loud tympanitic resonance is the rule through- 
out the affected side. Even a small amount of air is sufficient to ren- 
der the whole side tympanitic and often to obscure the dulness which 
the frequently associated pleural effusion would naturally produce. 
Indeed, it is the rule that small effusions are wholly masked by the 
adjacent tympany. 



268 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

In no other disease do we get snch clear, intense tympanitic 
resonance over the chest. 

The only exception to this rule occurs in cases in which the air 
within the chest is under great tension, making the chest walls so 
taut that, like an over- stretched drum, they cannot vibrate properly. 
Under these conditions the percussion note becomes muffled, at 
times almost dull. 

Areas of dulness corresponding to the displaced organs (heart 
or liver) may sometimes be percussed out. 

4. Auscultation. — Respiration and voice sounds are usually in- 
audible in the lower portions of the chest. At the top of the chest, 
and rarely in the lower parts, a faint amphoric or metallic breathing 
may be heard, but as a rule the amphoric quality is brought out 
much better by cough which is followed by a ringing after-echo. 
Or the air in the pleura may be set to vibrating and made to give 
forth its characteristic, hollow, ringing sound if a piece of metal 
{e.g., a coin) be placed on the back of the chest and struck with 
another coin, while we listen with the stethoscope over the front of 
the chest opposite the point where the coin is. 

The clear ringing sound heard in this way is quite different 
from the dull chink obtainable over sound lung tissue. 

The " falling- drop sound" or "metallic tinkle," and the lung 
fistula sound are occasionally audible (see above, p. 112). 

On the sound side the breath sounds are exaggerated. At the 
top of the affected side over the collapsed lung the breathing is 
bronchial and rales are occasionally heard. 

In the great majority of cases pneumothorax is complicated by 
an effusion of fluid in the affected pleural cavity and we have then 
the signs of 

III. Pneumohydrothorax or Pneumopyothorax. 

When both fluid and air are contained in the pleural cavity, the 
patient may himself be able to hear the splashing sounds which 
the movements of his own body produce. These are more readily 
appreciated if the observer puts his ear against the patient's chest 
and then shakes him briskly. Splashing sounds heard within the 



DISEASES AFFECTING THE PLEURAL CAVITY. 269 

chest are absolutely pathognomonic and point only to the combina- 
tion of fluid and air within the pleural cavity. One must distin- 
guish them, however, from similar sounds produced in the stomach. 
By observing the position of maximum intensity of the sounds, this 
distinction may be easily made. Unfortunately the critical condi- 
tion of the patient may make it impossible to try succussion, as in 
the acute cases with great shock it is dangerous to move him at all. 
The movements of breathing or coughing may bring out a " metal- 
lic tinkle " (see above, p. 112). At the base of the chest, over an 

Tuberculous so- 
**""' lidiflcation. 



Exaggerated 
resonance and " 
breathing. 

f Tympany ; 

{ absent voice ; 

-Air= < breathing ab- 

Displacedcardiac """ j\ [t^ZJ^(^/\ f^^T^ll] A ' ( sent or distant 

impulse. \ K\~V y/\ /\V vy7 / ' I amphoric. 

Dulness, shifting 
with change of po- 
sition = (fluid). 



Fig. 132.— Pneumohydrothorax with Displaced Heart. 

area corresponding to the position of the fluid, an area of dulness 
may be easily marked out by percussion, and this area shifts very 
markedly with change of position. The shifting dulness of pneu- 
mohydrothorax is strongly in contrast with the difficulty of obtain- 
ing any such shift in ordinary pleuritic effusion (see Fig 132) 

(The distinction between " open pneumothorax," in which the 
rent in the lung through which the air escaped in the pleura re- 
mains open, and "closed pneumothorax," in which the rent has 
become obliterated — is one which cannot be established by physi- 
cal signs alone. It is often said that amphoric breathing, and espe- 
cially an amphoric ring to the voice and cough sounds, denote an 




270 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

open pneumothorax, but post-mortem evidence does not bear this 
out. Practically an open pneumothorax is one in which the 
amount of effused air increases, and closed pneumothorax is one in 
which the physical signs remain stationary ) 

Differential Diagnosis 

The distinction between pneumothorax and emphysema has al- 
ready been discussed (see p. 260). 

(a) When the air in the pleural sac is under such tension that 
the percussion note is dull, the physical signs may simulate pleu- 
ritic effusion, but real flatness, such as characterizes effusion, has 
not, so far as I know, been recorded in pneumothorax, and the 
sense of resistance on percussing is much greater over fluid than 
over air. In case of doubt puncture is decisive. 

(b) Acute pneumothorax, coming on as it does with symptoms 
of collapse and great shock, may be mistaken for angina pectoris, 
cardiac failure, embolism of the pulmonary artery, or acute pulmo- 
nary tympanites (see above, p. 262). 

From all these it can be distinguished by the presence of am- 
phoric or metallic sounds, which are never to be obtained in the 
other affections named. 

(c) Hernia of the intestine through the diaphragm, or great 
weakening of the diaphragmatic muscular fibres, may allow the 
intestines to encroach upon the thoracic cavity and simulate pneumo- 
thorax very closely. The history and course of the case, the ab- 
dominal pain, vomiting, and indicanuria, generally suffice to distin- 
guish the condition. The peristalsis of the intestine may go on even 
in the thorax, and gurgling metallic sounds corresponding to it and 
unlike anything produced in the thorax itself may be audible 

The distinction between open and closed pneumothorax, to which 
I have already alluded, is far less important than the presence or 
absence of 

(a) Pulmonary tuberculosis 

(b) Encapsulating adhesions in which the air is confined to a 
circumscribed area 

(a) The examination of the sputa and of the compressed lung 



DISEASES AFFECTING THE PLEURAL CAVITY. 271 

may yield evidence regarding tuberculosis. On the sound side the 
compensatory hypertrophy covers up foci of dulness or rales so that 
it is difficult to make out much. 

(b) Encapsulated pneumothorax gives us practically all the signs 
of a phthisical cavity, from which it is distinguished by the fact 
that with a cavity the nutrition of the patient is almost always 
much worse. 

Encapsulated pneumothorax needs no treatment. Hence the 
importance of distinguishing it from the non-encapsulated form of 
the disease, in which treatment is essential. 

PLEURISY. 

Clinically, we deal with three types : 

(a) Dry or plastic pleurisy. 

(b) Pleuritic effusion, serous or purulent. 

(c) Pleural thickening. 

(a) Dry or Plastic Pleurisy. 

Doubtless many cases run their course without being recognized. 
The frequency with which pleuritic adhesions are found post mor- 
tem would seem to indicate this. 

It is usually the characteristic stitch in the side which suggests 
physical examination. The pain and the physical signs resulting 
from the fibrinous exudation are usually situated at the bottom of 
the axilla where the diaphragmatic and costal layers of the pleura 
are in close apposition. Doubtless the pleuritic inflammation is 
not by any means limited to this spot, but it is here that the two 
layers of the pleura make the largest excursion while in apposition 
with each other. In the vast majority of cases, then, the physical 
signs are situated at the spot indicated in Fig. 133. 

Occasionally pleuritic friction is to be heard in the precordial 
region, and after the absorption of a pleuritic effusion evidences 
of fibrinous exudation in the upper parts of the chest are sometimes 
demonstrable. Most rarely of all, evidence of plastic pleurisy may 
be found at the apex of the lung in connection with early phthisis. 
In diaphragmatic pleurisy, when the fibrinous exudation is espe- 



272 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



cially marked upon the diaphragmatic pleura, friction sounds may 
be heard over the region of the attachment of the diaphragm in 
front and behind as well as in the axillae. Hiccup often occurs and 
gives exquisite pain. 

Our diagnosis is based upon a single physical sign, pleuritic 
friction. The nature of this sound and the 
manoeuvres for eliciting it have already 
been described (see above, p. 108), and I 
will here only recapitulate what was there 
said. During the first few deep breaths 
one hears, while listening over the painful 
area, a grating or rubbing sound usually 
somewhat jerky and interrupted, most 
marked at the latter part of inspiration, 
but often audible throughout the whole 
respiratory act. After a few breaths it 
often disappears, but will usually reap- 
pear if the patient lies for a short time 
upon the affected side, and then sits up 
and breathes deeply. In marked cases 
the rubbing of the inflamed pleural sur- 
faces may be felt as well as heard, and it 
is not very rare for the patient to be able 
to feel and hear it himself. Pleuritic fric- 
tion may be present and loud without 
giving rise to any pain. On the other 
hand, the pain may be intense, and yet 
the friction-rub barely audible. When 
heard at the summit of the chest, as in 
cases of incipient phthisis, pleural fric- 
tion produces only a faint grazing sound, much more delicate and 
elusive than the sounds produced at the base of the chest, 

Occasionally the distinctive rubbing or grating sounds are more 
or less commingled with or replaced by crackling sounds indistin- 
guishable from the drier varieties of rales. It is now, I think, 
generally believed that such sounds may originate in the pleura as 




Fig. 133.— Showing the Point at 
which Pleural Friction is most 
Often Heard. 



DISEASES AFFECTING THE PLEURAL CAVITY. 273 

well as within the lung. The greatest care should be taken to 
prevent any shifting or slipping of the stethoscope upon the surface 
of the chest, as by such means sounds exactly like those of pleural 
friction may be transmitted to the ear. In case of doubt one 
should always wet or grease the skin so that the stethoscope can- 
not slip. 

Muscle sounds are sometimes taken for pleural friction, but they 
are bilateral, usually low-pitched, sound less superficial than pleu- 
ral friction, and are not increased by pressure. When listening 
for friction at the base of the left axilla, I have once or twice been 
puzzled by some low-pitched rumbling sounds occurring at the end 
of inspiration, and due (as afterward appeared) to gas in the stom- 
ach which shifted its position with each descent of the diaphragm. 

In children friction sounds and pleuritic pain are much less 
common than in adults, and the signs first recognizable are those 
of effusion. In adults the presence of a very thick layer of fat 
may make it difficult or impossible to feel or hear pleural friction. 

The breath sounds over the affected area are usually absent or 
greatly diminished, owing to the restraint in the respiratory move- 
ments due to pain. Not infrequently pleuritic friction may be 
heard altogether below the level of the lung. 

(b) Pleuritic Effusion. 

Many cases are latent, and the patients consult the physician on 
account of slight cough, weakness, or gastric trouble, so that the 
effusion is first discovered in the course of routine physical ex- 
amination. Since it is usually the results of percussion which first 
put us on the right track, I shall take up first 

Percussion. 

1. A small effusion first shows as an area of dulness 

(a) Just below the angle of the scapula. 

(b) In the left axilla between the fifth and the eighth rib. 

(c) Obliterating Traube's semilunar area of tympany; or 

(d) In the right front near the angle made by the cardiac and 
hepatic lines of dulness (see Fig. 134). 

18 



274 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

In the routine percussion of the chest, therefore, one should 
never leave out these areas. A small effusion is most easily de- 
tected in children or in adults with thin chest walls, provided our 
percussion is not too heavy. An effusion amounting to a pint 
should always be recognizable, and smaller amounts have frequently 
been diagnosed and proved by puncture. 

The amount of a pleuritic effusion is roughly proportional to 
the area of dulness on percussion, but not accurately. It is very 
common to find on puncture an amount of fluid much greater than 



Area of dulness 

due to small -<•-(- 

pleural effusion. "^-^ 




-1 Area of cardial 

dulness. 



Fig. 134.— Small Pleural Effusion Accumulating (in part) near the Right Border of the Heart. 



could have been suspected from the percussion outlines ; on the other 
hand, the dulness may be extensive and intense on account of great 
inflammatory thickening of the costal pleura, by the accumulation 
of layer after layer of fibrinous exudate and its organization into 
fibrous plates, while very little fluid remains within. 

The amount of dulness depends also upon the thickness and elasti- 
city of the chest wall and the degree of collapse of the lung within. 

2. Large Effusions. — When the amount of fluid is large, the dul- 
ness may extend throughout the whole of one side of the chest with 
the exception of a small area above the clavicle or over the primary 
bronchus in front. This area gives a high-pitched tympanitic note, 



DISEASES AFFECTING THE PLEURAL CAVITY. 



275 



provided the bronchi remain open, as they almost always do. This 
tympany is high-pitched and sometimes astonishingly clear. I re- 
cently saw a case in which the note above the clavicle was almost 
indistinguishable with the eyes shut from that obtained in the epi- 
gastrium. Occasionally " cracked-pot " resonance may be obtained 
in the tympanitic area. 

The pitch changes if the patient opens and closes his mouth 
while we percuss (''Williams' tracheal tone"). 

The dulness over the lower portions of a large effusion is usual- 
ly very marked, and the percussing finger feels a greatly increased 



Normal resonance 
and vesicular 
breathing. 



Tympany, voice and 
fremitus in- 
creased. 



Flatness, no breath- 
ing, voice sounds, 
or fremitus. 




Zone of condensed 
lung above the 
fluid. 



Exaggerated (com- 
pensatory) breath- 
ing and reso- 
nance. 



Fig. 135.— Diagram to Illustrate Physical Signs in Moderate-Sized Effusion in the Left Pleura. 



resistance to its blows when compared with the elastic rebound of 
the sound side. 

3. Moderate Effusions. — Three zones of resonance can often be 
mapped out in the back: at the base dulness or flatness, above 
that a zone of mingled dulness and tympany, and at the top normal 
resonance. The lowest zone corresponds to the fluid, the middle 
zone to the condensed lung immediately above it, and the top zone 
to the relatively unaffected part of the lung (see Fig. 135). Not 
infrequently there is no middle zone but simply dulness below and 
resonance above, as is usually the case in the axilla and front. 



276 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 



The position of the effusion depends only in part npon the in- 
fluence of gravity, and is greatly influenced by capillarity and the 
degree of retraction of the lungs* Consequently the surface of 
the fluid is hardly ever horizontal except in very large accumula- 
tions. With the patient in an upright position it usually reaches 
a higher level in the axilla than in the back. Near the spine and 
near the sternum (in right-sided effusions) the line corresponding 
to the level of the fluid may rise sharply. 

The S-curve of Ellis, as worked out so elaborately by Garland, 
varies still further the uneven line which corresponds to the sur- 



Triangular space 
dull until patient 
has coughed and 
breathed deeply. 



Area of dulness 
bounded above by 
the S-curve of 

Ellis. 



Fig. 136.— The S-Curve of Ellis. 

face of the fluid (see Fig. 136). This curve can be obtained only 
after the patient has, by cough and forced breathing, expanded the 
lung as fully as possible. 

All these curves are to be found with the patient in the upright 
position. None of them has any considerable diagnostic impor- 
tance, and the chief point to be remembered is that the upper sur- 
face of the fluid, not being settled by gravity alone, is hardly ever 
horizontal. 

With change in the position of the patient the level of the fluid 
sometimes changes very slowly and irregularly, and sometimes does 




DISEASES AFFECTING THE PLEURAL CAVITY. 277 

not change at all. If, for purposes of thorough, examination, we 
raise to a sitting posture a patient who has been for some days or 
weeks in bed, we should never begin the examination at once, since 
it may take some minutes for the lungs and the fluid to accommo- 
date themselves to the new position. It is well also to get the 
patient to cough and to take a number of full breaths before the 
examination is begun. 

To test the mobility of the fluid with change of the patient's 
position, mark out the upper limit of the dulness in the back with 
the patient in the upright position. Then let the patient lie face 
downward upon a couch, and, after waiting a few minutes, percuss 
the previously dull area. It may be found to have become resonant. x 

When the fluid is absorbed or removed by tapping, one would 
expect an immediate return of the percussion resonance. But in 
fact the resonance returns very slowly and is wholly unreliable as 
a test of the amount of absorption which has occurred. Thickened 
pleura and atelectatic lung may abolish resonance long after the 
fluid is all gone. TTe depend here far more upon the evidence ob- 
tained by auscultation and palpation and on the general condition 
of the patient. 

To determine the returning elasticity of the lung and the degree 
of movability of its lower border, percussion is very useful during 
the stage of absorption. After percussing out the lower border of 
pulmonary resonance in the back, the patient is directed to take a 
long breath and hold it. If the lung expands, the area of percus- 
sion resonance will increase downward. 

Percussion aids us in determining whether neighboring organs 
are displaced by the pressure of the accumulated fluid. The liver 
is often pushed down, the spleen very rarely. Dislocation of the 
heart is one of the most important of all the signs of pleural effu- 
sion, and is often the crucial point in differential diagnosis. It is 

1 This test, however, is somewhat fallacious and of very little diagnostic 
value, since the lungs tend to swing up toward the back when the patient lies 
prone, even when no fluid is present, and increase of resonance in the back with 
this change of position might, therefore, occur when the dulness was due to 
thickened pleura and not to fluid. 



278 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

a very striking and at first surprising fact that a left-sided effusion 
displaces the heart far more than a right- sided effusion of the same 
size. Small or moderate right-sided effusions often do not displace 
the heart at all. 

"With left-sided effusions, unless very small, we find the area of 
cardiac dulness shifted toward the right and often projecting be- 
yond the right edge of the sternum (see Fig. 134). (Inspection and 
palpation often give us even more valuable information on this 
point. See below, p. 281.) We must be careful to distinguish such 
an area of dulness at the right sternal margin from that which may 
be produced in right-sided effusions by the fluid itself (see above). 

As mentioned abo\'e, a right pleural effusion may very early 
show itself as an area of dulness along the right sternal margin. 
Light percussion will usually demonstrate that this dulness is con- 
tinuous with a narrow strip of flatness at the base of the axilla 
(ninth and tenth ribs). Such an effusion is late in creeping up the 
axilla. It appears first and disappears first along the right margin 
of the sternum. 

On the sound side the percussion resonance is often increased, 
owing to compensatory hypertrophy of the sound lung ; the dia- 
phragm is pushed down and the borders of the heart or of the liver 
may be encroached upon. When the hyper-resonance of the sound 
side is present, it should warn us to percuss lightly over the effu- 
sion, else we may bring out the resonance of the distended lung. 

Summary of Percussion Signs. — (1) Flatness corresponding 
roughly to the position of the fluid. 

(2) Tympany above the level of the fluid over the condensed 
lung. 

(3) The level of the fluid is seldom quite horizontal. 

(4) Shifting of the fluid with change of position is rare, slow, 
and has little or no importance in diagnosis. 

Exceptions and Possible Errors. — (a) Great muscular pain and 
spasm may produce an area of dulness which simulates that of 
pleural effusions, especially as the auscultatory signs may be equally 
misleading. A hypodermic of morphine will dispel the dulness 
along with the pain if it is due to muscular cramp. 



DISEASES AFFECTING THE PLEURAL CAVITY. 279 

(b) If the lung on the affected side fails to retract (owing to 
emphysema or adhesions to the chest wall), the area of dulness and 
its intensity will be much diminished. 

(c) It must be remembered that dulness in Traube's space may 
be due to solidification of the lung, to tumors, or to overfilling 
of the stomach and intestine with food, as well as to pleural effu- 
sion ; also that the size of the tympanitic space varies greatly in 
health. 

(d) Rarely percussion may be tympanitic over an effusion at 
the left base owing to distention of the stomach or colon. 

(e) The diagnosis between fluid and thickened pleura will be 
considered later. 

Auscultation. 

The auscultatory phenomena vary greatly in different cases, and 
in the same case at different times, because the essential condi- 
tions are subject to similar variations. Whatever sounds are pro- 
duced in the kings or in the bronchi may be heard over the fluid un- 
less interfered with by inflammatory thickening of the costal pleura. 
Fluid transmits sounds well, but there may be no breath sounds pro- 
duced and hence none audible over the fluid. Or tubular sounds 
only may be produced because only the bronchi remain open, the 
rest of the lung being collapsed. 

Or again, if rales or friction sounds are produced in the lung, 
they, too, may be transmitted to the fluid and may (alas!) deter 
the timid " observer " from tapping. 

In about two-thirds of all large effusions no breathing at all is 
audible over the area of flatness on percussion. In the remaining 
third, and especially in children, tubular breathing, sometimes 
feeble, sometimes very intense, is to be heard.. 

In moderate effusions there are often three zones in the back 
At the bottom we hear nothing, in the middle zone distant bron- 
chial or broncho-vesicular breathing, while at the summit of the 
chest the breathing is normal. 

The voice sounds correspond When breath sounds are absent, 
the voice sounds are likewise absent When the breathing is tubu- 



280 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

lar, the voice, and especially the whisper, is also tubular and inten- 
sified. That is, whenever the bronchi are open, the lung retracted, 
and the chest walls thin, the breathing, voice, and whisper will corre- 
spond to the tracheal and bronchial sounds. Since children have es- 
pecially thin chest walls, these bronchial sounds are especially fre- 
quent and intense in children. 1 

Near the angle of the scapula and in a corresponding position 
in front, the sound of the spoken voice may have a peculiar high- 
pitched, nasal twang, to which the term egophony is applied. 
This sign has no importance in diagnosis, since it is not constant, 
and not peculiar to fluid accumulations. 

Kales are rarely produced in the retracted lung, and so are 
rarely to be heard over the fluid. 

All these sounds may be diminished or abolished if the costal 
pleura is greatly thickened 

The influence of cough upon the lung, and so upon the sounds 
produced in it and transmitted through the fluid, may be very great 
and very puzzling- Rales may appear or disappear, breathing 
change in quality or intensity, and in the differential diagnosis of 
difficult cases the patient should always be made to cough and then 
breathe deeply before the examination is completed. 

In very large effusions, when only the primary bronchi are 
open, there may be signs like those of pulmonary cavity at the site 
of the bronchi in front or behind (amphoric breathing, large metallic 
rales, etc.). Over the sound lung the breathing is exaggerated and 
extends unusually far down in the back and axilla, owing to hyper- 
trophy of the lung. 

The heart sounds may be absent at the apex owing to disloca- 
tion of the heart. In left-sided effusions the apex sounds are often 
loudest near the ensiform cartilage or beyond the right margin of 
the sternum. Eight-sided effusions have much less effect upon the 
heart, but occasionally we find the heart sounds loudest at the left 
of the nipple or in the axilla. 

Since many cases of pleural effusion are due to tuberculosis, we 

'Bacelli's theory — that the whispered voice is conducted through serum 
but not through pus — is not borne out by facts. 



DISEASES AFFECTING THE PLEURAL CAVITY. 281 

should never omit to search, for evidences of this disease at the 
apex of the lung on the sound side, since experience has shown that 
phthisis is more apt to begin here than on the side of the effusion. 

Summary of Auscultatory Signs. 

(1) In most cases voice and breath sounds are absent or very 
feeble over the area occupied by the fluid. 

(2) In a minority of the cases the breathing and voice sounds 
may be tubular and intensified, especially in children. 

(3) Over the condensed lung at the summit of the chest the 
breathing is bronchial or broncho-vesicular, according to the degree 
of condensation. If the amount of fluid is small, the layer of con- 
densed lung occupies the middle zone of the chest and the breath- 
ing is normal at the top of the chest. 

(4) Rales and friction sounds are rarely heard over fluid. 

(5) On the sound side the breathing is exaggerated. 

(6) The heart sounds may be absent at the apex and present in 
the left axilla or to the right of the sternum owing to dislocation 
of the heart. 

Inspection and Palpation. 

The most important information given us by inspection and 
palpation relates to the displacement of various organs by the pres- 
sure of the accumulated fluid. In left-sided pleuritic effusions the 
heart is usually displaced considerably toward the right, even when 
the level of the fluid reaches no higher than the sixth rib in the 
nipple line. The apex impulse is to be seen and felt to the right 
of the sternum, somewhere between the third and the seventh rib, 
when a large amount of fluid is present. With smaller effusions 
one may find the apex beat lifting the sternum or close to its left 
border. The position of the heart may be confirmed by percussion. 

The spleen is scarcely ever displaced. 

Right-sided effusions are far less likely to displace the heart, and 
it is only when a large amount of fluid is present that the apex of 
the heart is pushed outward beyond the nipple. Moderate right- 
sided effusions often produce no dislocation of the heart whatever. 
The liver is often considerably pushed down by a right-sided pleu- 



282 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

ritic effusion, and its edge may be palpable several inches below the 
costal margin. Its upper margin cannot be determined by percus- 
sion, as it merges into the flatness produced by the fluid accumula- 
tion above it. 

Tactile fremitus is almost invariably absent or greatly dimin- 
ished over the areas corresponding to the fluid ; just above the level 
of the fluid it is often increased. 

Occasionally a slight fulness of the affected side may be recog- 
nized by inspection, and the interspaces may be less readily visible 
than upon the sound side. Bulging of the interspaces I have never 
observed. When the accumulation of fluid is large the respiratory 
movements upon the affected side are somewhat diminished, 1 the 
shoulder is raised, and the spine curved toward the affected side. 
The diaphragm is depressed, and Litten's sign therefore absent. 

There are no reliable means for distinguishing purulent from 
serous effusions. The whispered voice may be transmitted through 
either pus or serum. But we know that in children two-thirds of 
all effusions are purulent, while in adults three-fourths of them are 
serous. 

Physical Signs During Absorption of Pleural JEffusions. 

When the fluid begins to disappear, either spontaneously or as 
a result of treatment, the dulness very gradually disappears and 
the breath sounds, voice sounds, and fremitus reappear. In case 
the heart has been dislocated, its return to its normal position is 
often much slower than one would anticipate, and indeed all the 
physical signs are disappointingly slow to clear up even after tap- 
ping. Pleural friction appears when the roughened pleural surfaces, 
which have been held apart by the fluid, are allowed by the disap- 
pearance of the latter to come into apposition again. Owing to pul- 
monary atelectasis and permanent thickening of the pleura, con- 
siderable dulness often remains for weeks after the fluid has been 
absorbed. 

1 1 have purposely made but little of the changes in the shape of the chest 
produced by pleuritic effusions, as it has seemed to me that by far too much 
stress has usually been laid upon such signs. 



DISEASES AFFECTING THE PLEURAL CAVITY. 283 

(c) Pleural Thickening. 

In persons who have previously suffered from pleurisy with 
effusion, and in many who have never to their knowledge had any 
such trouble, a considerable thickening of the pleural membrane 
with adhesion of the costal and visceral layers may be manifested 
by the following signs : 

(1) Dulness on percussion, sometimes slight, sometimes marked. 

(2) Diminished vesicular respiration. 

(3) Diminished voice sounds and tactile fremitus. 

(4) Absence of Litten's phenomenon and diminution in the 
normal respiratory excursion of the chest. 

These signs are most apt to be found at the base of the lung 
behind and in the axilla. Occasionally a similar thickening may 
be demonstrated throughout the whole extent of the pleura, and the 
lung failing to expand, the chest may fall in as a result of atmos- 
pheric pressure (see Fig. 20). 

The ribs approximate and may overlap, the spine becomes 
curved, the shoulder lowered, the scapula prominent, and the whole 
side shrunken. The heart may be drawn over toward the affected 
side. 

In the diagnosis of pleural thickening Rosenbach's "palpatory 
puncture " is sometimes our only resource. Under antiseptic pre- 
cautions a hollow needle is pushed between the ribs and into the 
pleural cavity. As the needle forces its way through the tough 
fibrous, or perhaps calcified, pleura, the degree and kind of resist- 
ance are very enlightening. Again, the amount of mobility of the 
point after the chest wall has been pierced tells us whether the 
needle is free in a cavity, entangled in a nest of adhesions, or fixed 
in a solid " carnified " lung. There is no danger if the needle is 
sterile. 

Encapsulated Pleural Effusion. 

Small accumulations of serum or pus may be walled off by ad- 
hesions so that the fluid does not gravitate to the lowest part of 
the pleural cavity or spread itself laterally as it would if free. 



284 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Such localized effusions are most apt to be found in the lower axil- 
lary regions or behind — sometimes between the base of the lung and 
the diaphragm, and more rarely between the lobes of one of the 
lungs or higher up. I have twice seen an encapsulated purulent 
effusion so close to the left margin of the heart that the diagnosis 
of pericardial effusion was made. 

The diagnosis of encapsulated pleural effusion is a difficult one 
and oftentimes cannot be made except by puncture. The signs are 
those of fluid in the pleura, but anomalously placed. Even punc- 
ture may fail to clear up the difficulty, since the needle may pass 
entirely through the pouch of fluid and into some structure behind 
so that no fluid is obtained. 

Pulsating Pleurisy (Empyema Necessitatis). 

Under conditions not altogether understood the movements 
transmitted by the heart to a pleural effusion (usually purulent) 
may be visible externally as a circumscribed pulsating swelling near 
the precordial region, or as a diffuse undulation of a considerable 
portion of the chest wall. Sometimes this pulsation is visible be- 
cause the fluid has worked its way out through the thoracic wall 
and is covered only by the skin and subcutaneous tissues, but occa- 
sionally pulsation in a pleural effusion becomes visible, although no 
such perforation of the chest wall has occurred. 

The condition is a rare one, and is of importance only because it 
may be mistaken for an aneurism, from which, however, it should 
be readily distinguished by the absence of a palpable thrill or dias- 
tolic shock and by the evidence of fluid in the pleura. 

Differential Diagnosis of Pleuritic Effusion. 

The following conditions are not infrequently mistaken for 
pleuritic effusion : 

(1) Croupous pneumonia with occlusion of the bronchi. 

(2) Pleural thickening, with pulmonary atelectasis. 

(3) Subdiaphragmatic abscess or abscess of the liver. 

In croupous pneumonia with plugging of the bronchi one may 



DISEASES AFFECTING THE PLEURAL CAVITY. 285 

have present all the physical signs of pleuritic effusion except dis- 
placement of the neighboring organs. The presence or absence of 
such displacement, together with the history, symptoms, and course 
of the case, is therefore our mainstay in distinguishing the two 
diseases. 

From ordinary croupous pneumonia (without occlusion of the 
bronchi) pleuritic effusion differs in that it produces a greater de- 
gree of dulness and a diminution of the spoken voice sounds and 
tactile fremitus. Bronchial breathing and bronchial whisper may 
be heard either over solid lung or over fluid accumulation, although 
the bronchial sounds are usually feeble and distant in the latter 
condition. The displacement of the neighboring organs is of im- 
portance here as in all diagnoses in which pleuritic effusion is a 
possibility. In pleuritic effusion we can sometimes determine that 
the line marking the upper limit of dulness shifts with change of 
the patient's position. This is, of course, impossible in pneumo- 
nia. A few hard coughs may open up an occluded bronchus and 
so clear up the diagnosis at once. In doubtful cases the patient 
should always be made to cough and breathe deeply before the 
examination is finished. 

It should always be remembered that one may have both pneu- 
monia and pleuritic effusion at the same time, and that pneumonia 
is often followed by a purulent effusion. In children the bronchi 
are especially prone to become occluded even as a result of a simple 
bronchitis, and we must then differentiate between atelectasis and 
effusion — in the main by the use of the criteria just described. 

(2) It is sometimes almost impossible to distinguish small fluid 
accumulations in the pleural cavity from pleural thickening with 
pulmonary atelectasis. In both conditions one finds dulness, dimi- 
nution of the voice sounds, respiration, and tactile fremitus, and 
absence of Litten's phenomenon, but the tactile fremitus is usually 
more diminished when fluid is present than in simple pleural thick- 
ening and atelectasis. An area of dulness which shifts with change 
of position points to pleuritic effusion. The presence of friction 
sounds over the suspected area speaks strongly in favor of pleural 
thickening, but it is possible to hear friction sounds over fluid, 



286 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

probably because they are conducted from a point higher up in the 
chest at which no fluid is present. In doubtful cases the diagnosis 
can and should be cleared up by puncture. 

(3) In two cases I have known enlargement of the liver due tc 
multiple abscesses to be mistaken for empyema. In both condi- 
tions, one finds in the right back dulness on percussion as high as 
mid-scapula, with absence of voice sounds, breath sounds, and 
fremitus. These conditions are due in one case to the presence of 
fluid between the lung and the chest wall, and in the other case to 




Fig. 137.— Area of Dulness in Solitary (tropical) Abscess of the Liver. 

the liver which pushes up the lung together with the diaphragm. 
By physical signs alone I do not see how this diagnosis is possible, 
though Litten's sign may be of use, since the shadow is absent 
in empyema and sometimes present in moderate-sized subdia- 
phragmatic accumulations. Some of the symptoms, such as chills , 
sweating, and irregular fever, are common to both conditions. A 
careful consideration of the history and the associated signs and 
symptoms may help us to decide. 

Large solitary abscess of the liver, occurring as it almost in- 
variably does in the posterior portion of the right lobe, produces an 
area of flatness on percussion, which rises to a much higher level in 



DISEASES AFFECTING THE PLEURAL CAVITY. 287 

the axilla and back than in front or near the stermim (see Fig. 137), 
and may be in this way distinguished from empyema; but when the 
liver contains many small abscesses, as in suppurative cholangitis, 
this peculiar line of dulness is not present. 

(d) Kare diseases, such as cancer or hydatid of the lung, may 
be mistaken for pleuritic effusion. The history of the case and the 
results of exploratory puncture usually clear up the difficulty. 



CHAPTER XIV. 

ABSCESS, GANGRENE, AND CANCER OE THE LUNG, 
PULMONARY ATELECTASIS, (EDEMA, AND HYPO- 
STATIC CONGESTION. 

Abscess axd Gangrene of the Lung. 

I consider these two affections together because the physical 
signs, exclusive of the sputa, clo not differ materially in the two 
affections. In some cases there may be no physical signs at all, 
and the diagnosis is made from the character of sputa and from a 
knowledge of the etiology and symptomatology of the case. In 
other cases we find nothing more than a patch of coarse rales or a 
small area of solidification, over which distant bronchial breathing, 
with increased voice sound and fremitus, may be appreciated. 
Rarely there may be slight dulness on percussion, but as a rule the 
area is not sufficiently large or sufficiently superficial to produce 
this. One may find the signs of cavity (amphoric breathing, 
cracked-pot resonance, and gurgling rales), but this is unusual. 

Gangrene of the lung is not a common disease. The diagnosis 
usually rests altogether upon the smell and appearance of the sputa. 
In fetid bronchitis one may have sputa of equal foulness, but the 
odor is different. The finding of elastic tissue in the sputa proves 
the existence of something more than bronchitis. 

Pulmonary abscess, which, like gangrene, is a rare affection, is 
often simulated by the breaking of an empyema into the lung and 
the emptying of the pus through a bronchus. Large quantities of 
pus are expectorated in such a condition, and abscess of the lung is 
suggested, but the other physical signs are those of empyema and 
should be easily recognized as such. The finding of elastic fibres 
is the crucial point in the diagnosis of intrapulmonary abscess, 



ABSCESS, GANGRENE, AND CANCER OF THE LUNG. 289 

whether due to the tubercle bacillus or to other organisms. Tuber- 
culous abscess (cavity) is usually near the summit of the lung, and 
other varieties of abscess are near the base, but often there are 
no physical signs by which we can distinctly localize the process. 

Maligxaxt Disease of the Luxg. 

In its earlier stages this affection is often mistaken for empy- 
ema or serous effusion in the pleural cavity, and indeed the physi- 
cal signs may be in part due to an accumulation of fluid secondary 
to the malignant growth within the lung. The rapid emaciation 
of the patient and the presence of a dark-brown bloody fluid in the 
pleural cavity, as determined by puncture, make us suspect ma- 
lignant disease. The sputa rarely contain fragments of tissue 
whose structure can be recognized as characteristic of malignant 
disease. Secondary deposits in the supraclavicular glands may 
suggest the diagnosis. 

The thorax is usually somewhat asymmetrical. The affected 
side may be either contracted or distended according to the nature 
of the malignant growth within ; occasionally it is not deformed at 
all. When the growth attacks only the lung tissue itself, leaving 
the bronchi and mediastinum free, we get signs like those of pleu- 
ral effusion (flatness, absent breathing, voice sounds, and tactile 
fremitus), but the line of dulness is apt to be higher in front than 
behind, which is rarely the case in pleural effusion. 

If the disease begins in the bronchi, we may have a noisy dysp- 
noea from stenosis of a bronchus, and a weakening of the respiratory 
sounds normally to be heard over the trachea in front has several 
times been noted. Percussion dulness, if present, is usually over 
the upper portions of the chest, and may disappear and reappear 
or skip from place to place in a very irregular and confusing way. 

Signs and symptoms of pressure in the mediastinum due to sec- 
ondary involvement of the peribronchial glands may be present and 
may simulate aneurism, but with aneurism the cachexia is usually 
less marked. 
19 



290 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

Atelectasis. 

(a) Areas of atelectasis or collapse of pulmonary tissue are 
often present in connection with various pathological processes in 
the lung (such as tuberculosis or lobular pneumonia), but are usu- 
ally too small to give rise to any characteristic physical signs; 
nevertheless 

(5) In most normal individuals a certain degree of atelectasis 
of the margins of the lungs may be demonstrated in the following 
way : The position of the margins of the lungs in the axillae, in the 
back, or in the precordial region are marked out by percussion at the 
end of expiration. The patient is then directed to take ten full 
breaths, and the pulmonary outlines at the end of expiration are 
then percussed out a second time. The pulmonary resonance will 
now be found to extend nearly an inch beyond its former limits, 
owing to the distention of previously collapsed air vesicles. 

If one auscults the suspected areas during the deep breaths 
which are used to dispel the atelectasis, very fine rales are often 
to be heard at the end of expiration, disappearing after a few 
breaths in most cases, but sometimes audible as long as we choose 
to listen to them. These sounds, to which Abrams has given the 
name of " atelectatic crepitation," are in my experience especially 
frequent at the base of either axilla. The same writer has noticed 
an opacity to the arrays over such atelectatic areas. 

Forcible percussion may be sufficient to distend small areas of 
collapsed lung, or at any rate to dispel the dulness previously pres- 
ent (see above, p. 76, the lung reflex). 

(c) ~S\ "hen one of the large bronchi is compressed (as by an 
aneurism) or occluded by a foreign body, collapse of the corre- 
sponding area of lung may be shown by diminished motion of the 
affected side, dulness on percussion, and absence of breathing, voice 
sounds, and tactile fremitus. 

In new-born babies whose lungs do not fully expand at the time 
of birth, similar physical signs are present over the non-expanded 
lobes. The right lung is especially apt to be affected 

In the differential diagnosis of extensive pulmonary collapse, 



ATELECTASIS, GEDEMA, AND HYPOSTATIC CONGESTION. 291 

the etiology, the suddenness of their onset, the absence of fever and 
of displacement of neighboring organs enable us to exclude pneu- 
monia and pleuritic effusion. 

(Edema of the Lungs. 

In cardiac or renal disease one can often demonstrate that the 
lungs have been invaded by transuded serum as a part of the gen- 
eral dropsy. More rarely pulmonary oedema exists without much 
evidence of oedema in other organs or tissues. 

The only physical sign characteristic of this condition is the 
presence of fine moist rales in the dependent portions of the lungs; 
that is, throughout their posterior surfaces when the patient has 
been for some time in a recumbent position ; or over the lower por- 
tions of the axillae and the back if the patient has not taken to 
his bed. 

The rales are always bilateral (unless the patient has been lying 
for a long time on one side), and the individual bubbles appear to 
be all of the same size, or nearly so, differing in this respect from 
those to be heard in bronchitis. No squeaking or groaning sounds 
are to be heard. The respiratory murmur is usually somewhat 
diminished in intensity. 

Dulness on percussion and modification of voice sounds are not 
present, unless hydrothorax or hypostatic pneumonia complicate 
the oedema. 

Hypostatic Pneumonia. 

In long, debilitating illness, such as typhoid fever, the alveoli 
of the dependent portions of the lungs may become so engorged 
with blood and alveolar cells as to be practically solidified. Under 
these conditions examination of the posterior portions of the lungs 
shows usually : 

(a) Slight dulness on percussion reaching usually from the 
base to a point about one-third way up the scapula. At the very 
base the dulness is less marked and becomes mixed with a shade of 
tympany. 

(b) Feeble or absent tactile fremitus. 



292 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(c) Diminished or suppressed breathing and voice sounds. 

The right lung is apt to be more extensively affected than 
the left. 

Occasionally the breathing is tubular and the voice sounds are in- 
creased, making the physical signs identical with those of croupous 
pneumonia, but as a rule the bronchi are as much engorged as the 
alveoli to which they lead, and hence no breath sounds are pro- 
duced. 

Rales of oedema or of bronchitis may be present in the adjacent 
parts of the lungs. The fact that the dulness is less marked at the 
base of the lung than higher up helps to distinguish the condition 
from hydrothorax. 

The diagnosis is usually easy, owing to the presence of the un- 
derlying disease. Fever, pain, and cough such as characterize 
croupous pneumonia are usually absent. 



APPENDICES. 



APPENDIX A. 

DISEASES OF THE MEDIASTINUM 

I. Mediastinal Tumors. 

New growths of the mediastinal glands 1 usually manifest their 
presence by the following symptoms and signs : 

(1) Cachexia and substernal pain. 

(2) Evidence of pressure against : — 

(a) The gullet. 

(b) The luindjjipe or primary bronchi. 

(c) The large venous trunks. 

{d) Nerves which pass through the mediastinum. 

(e) The subclavian arteries. 

(/) The heart. 

(g) The ribs, clavicle, or sternum. 

(3) Secondary deposits in the cervical or axillary glands. 

(a) By pressure on the gullet swallowing may be rendered diffi- 
cult or impossible (dysphagia). 

(b ) By pressure on the windpipe may be produced displacement 
of the latter to one side, or fixation so that it cannot be moved in 
any direction. The larynx may be drawn down into a noticeably 
low position, and the laryngoscope may demonstrate that the tra- 
cheal wall is bulged inward by the pressure of the new growth 
upon it. 

Dyspnoea, either inspiratory or expiratory, or both, and often 

1 Tuberculous glands not being here included. 



294 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

of noisy strident type, may result from stenosis of the trachea or 
primary bronchi. Owing to pressure on one of the large bronchi, 
the resonance and breath sounds' and fremitus may be diminished 
over the corresponding lung, in which finally abscess or gangrene 
may develop, owing to the retention and decomposition of the 
bronchial secretions. 

(c) If the pulmonary veins are pressed upon, a systolic murmur 
may be audible in the left back, and congestion of the lungs may 
ensue. 

Pressure on the innominate and subclavian veins produces cya- 
nosis or oedema of the head, neck, shoulder, and arm, while the 
superficial veins of the chest may become enlarged and prominent 
owing to an attempt at collateral circulation, especially if the vena 
cava superior is pressed upon. Fluid may accumulate in one or 
both pleural cavities if the vena azygos or thoracic duct is in- 
volved. 

(d) Aphonia or hoarseness points to pressure on the recurrent 
laryngeal nerve, and on laryngoscopic examination one vocal cord 
may be found in the cadaveric position. Inequality of the pupils, 
due to pressure on the sympathetic nerves, is not uncommon, and 
severe pain along the distribution of the intercostals or running 
down the arm indicates that the spinal ganglia or brachial plexus 
are pressed upon. Much rarer are symptoms of pressure on the 
vagus (slowing or quickening of the heart) and on the phrenic 
nerve (hiccup, unilateral spasm, or paralysis of the diaphragm). 

(e) Weakening or delay in one radial pulse maybe due to press- 
ure on the subclavian artery. 

(/) Occasionally the heart itself may be pushed out of place. 

{g) Pressure of the new growth against the bones of the chest 
may give rise to an area of percussion dulness over or near the 
manubrium, which, however, is not likely to show itself until late 
in the course of the disease when the new growth has reached a 
considerable size. In many cases there is tympanitic resonance in- 
stead of dulness over the affected area. The ribs or sternum may 
be pushed forward, but this is not usually the case. Occasionally 
the new growth, if very vascular, may pulsate like an aneurism or 



DISEASES OF THE MEDIASTINUM. 295 

transmit the pulsations of the heart to the chest wall, and a systo- 
lic murmur may be heard over the pulsating area, so that the resem- 
blance to aneurism is increased. 

D iffe i •ential Diagnosis . 

Mediastinal tumors may be mistaken for 

(1) Aneurism of the aortic arch. 

(2) Syphilitic stenosis of a bronchus. 

(3) Phthisis. 

Aneurism may be confounded with mediastinal new growths 
even by the most competent observers. Tactile thrill, diastolic 
shock, and tracheal tugging, if present, should suggest aneurism. 
If these signs are absent, aneurism may still be present but cannot 
be surely diagnosed. The degree of ansemia and emaciation is usu- 
ally greater in malignant disease than in aneurism, but this is not 
always the case. The presence of secondary nodules in the neck or 
armpit speaks strongly in favor of new growth. 

Stenosis of a bronchus, due to syphilis and giving rise to dysp- 
noea, cough, stridor, pulmonary atelectasis, may be very difficult to 
distinguish from mediastinal growth, but the degree of anaemia and 
emaciation is usually less in syphilis, and the beneficial results of 
antisyphilitic treatment may render the diagnosis possible, espe- 
cially if there is evidence of syphilis elsewhere in the body or in 
the history of the case. 

Phthisis may be suggested by the weakness, emaciation, and 
persistent cough produced by mediastinal growths, but should be 
easily excluded by the examination of the lungs and sputa. 

II. Mediastinitis. 

The acute suppurative forms of this rare disease do not give rise 
to any characteristic physical signs in the chest. 

The evidences of chronic fibrous mediastinitis have been already 
sufficiently considered in connection with adhesive pericarditis. 



296 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST 

III. Tuberculosis of the Mediastinal Glands. 

Probably every case of pulmonary tuberculosis is preceded or 
accompanied by tuberculosis of the bronchial lymph glands, and in 
numberless cases the tuberculous process never gets beyond these 
glands but is choked off there. In post-mortem examinations of 
children, no matter what the cause of death, it is exceptional not 
to find the bronchial glands tuberculous. 

Nevertheless the disease can but rarely be recognized during 
life. We may suspect it if, in a child showing tuberculous cervical 
glands or phthisis, we find evidence of pressure upon the right 
bronchus, increased tactile fremitus above the manubrium, lateral 
displacement of the trachea, or weakening of the pulse during in- 
spiration. If a bronchus is compressed, the resonance, tactile 
fremitus, and breath sounds are diminished over the correspond- 
ing lung. Wiederhofer lays stress upon an increase in the inten- 
sity of the expiratory murmur over the situation of the left primary 
bronchus. 



APPENDIX B. 
ACUTE ENDOCARDITIS. 

Whether the disease be of the benign or of the malignant (sep- 
tic) type, the results of physical examination of the heart are usu- 
ally very equivocal. We may guess that endocarditis is present 
owing to the presence of a cause (rheumatism), of a fever not oth- 
erwise explained, of a rapid irregular pulse of low tension, but the 
physical signs over the heart will not usually assist our guess ma- 
terially. 

Murmurs are often present but have usually the characteristics 
of " functional " murmurs (systolic, limited, soft, without accentu- 
ation of the pulmonic second sound or cardiac enlargement). If 
we can observe the advent of a diastolic murmur in such a case, we 
may fairly attribute it to a fresh endocarditis of the aortic (very 
rarely of the pulmonic) valve, but if we have not had the oppor- 



PHYSICAL EXAMINATION OF THE CHEST IN INFANTS. 297 

trinity to examine the heart previous to the onset of the present 
attack it is impossible to exclude a long-standing valvular lesion as 
the cause of the murmur. 

If murmurs come and go from day to day, or suddenly increase 
in intensity, we may suspect an acute endocarditis, especially if a 
musical murmur is present or if there be evidence of embolism. 

Inspection, palpation, and percussion usually yield no signs of 
importance. There is no enlargement of the heart, no accentuation 
of the second sounds, and no evidence of stasis. 



APPENDIX C. 

PHYSICAL EXAMINATION OF THE CHEST IN INFANTS. 

(1) Tactile fremitus and voice sounds can be investigated only 
in case the child cries or crows. The cry-souncl is intensified over 
solidified areas and may or may not be lost over fluid accumula- 
tions. 

(2) Percussion must be very delicately performed if we are to 
avoid setting the whole chest in vibration with every stroke. It is 
best to strike wholly with the finger, keeping the hand (as well as 
the wrist and arm) unmoved. 

(3) In listening to an infant's lungs patience and concentration 
are essential. The child is apt to stop breathing when the exami- 
nation begins, and we have to wait patiently to catch the long-de- 
layed inspiration " on the wing, " as it were, before the long expi- 
ratory wail begins. Luckily the inspiration, when it does come, is 
unusually intense owing to the thinness of the chest in infancy. 

(4) Long flexible rubber tubes connecting the chest-piece of the 
stethoscope with the ear-pieces are very convenient when examin- 
ing a wriggling child (see Fig. 48, p. 79), as they make it possible 
to hold the chest-piece in position despite the constant movements 
of the struggling sufferer. 

(5) It is advisable to examine first the back while the child is 
held in the mother's arms with its back to the physician. 



298 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

(6) Children almost always cry if made to lie down flat. If 
we wish to bring out the cry sound in order to test the vocal and 
tactile fremitus, this is a simple and humane method of producing 
it. If, on the other hand, peace is what we most desire, it is best 
to avoid putting the child in a recumbent position. 

(7) There is no type of breathing peculiar to children or in- 
fants. Puerile breathing is simply vesicular breathing heard very 
distinctly on account of the thinness of the chest. If, in a healthy 
child, the expiratory murmur is prolonged and high-pitched, this is 
probably because the child blows out the breath forcibly in the 
effort to breathe deeply as it is told to do. A young infant never 
does this, and its breathing is like that of adults except that it is 
more rapid, more irregular, and better heard. 



APPENDIX D. 

RADIOSCOPY OF THE CHEST. 

Radioscopy gives assistance in the diagnosis of diseases of the 
chest in two ways : 

1. Through the use of the fluoroscopic screen. 

2. Through the use of radiographs. 

Those who are accustomed to the use of the fluoroscope gain 
far more information from it than from radiographs, but the record 
of the photographic plate is objective, permanent, and demon- 
strable, while the impressions gained from the fluoroscope are more 
apt to be modified by the personal equation. 

For the present, therefore, we need both methods. 

I shall not attempt to discuss the advantages of the various 
forms of apparatus used for producing Roentgen rays in a Crookes 
tube ; the subject would carry me beyond my depth as well as be- 
yond the limits of this book ; but whatever form of instrument is 
used, the vacuum in the tube should be less perfect when we desire 
to use it for the chest than when searching for foreign bodies or 
studying fractures. We need a "low " or " soft " tube which gives 



RADIOSCOPY OF THE CHEST. 299 

rays of a relatively slight degree of penetration. With high pene- 
tration rays the outlines of the solid organs are less distinct because 
the rays traverse the heart and liver almost as easily as they do tlte 
lungs. If the penetrating power is less, the rays are arrested by 
the solid organs, but not by the lungs, and hence the outlines of the 
former become visible. 

I. The Use of the Fluoroscope. 

1. It is advisable to remain in a dark room or to wear smoked 
glasses for a short time before attempting to use the fluoroscope. 
This applies especially to beginners. Skilled observers do not need 
such preparation of the retina, but many novices who complain at first 
that they can " see absolutely nothing " when they apply the fluoro- 
scope to the chest, find their vision suddenly and permanently im- 
proved after fifteen minutes in a dark room. Practice increases our 
powers with the fluoroscope as much as it does with the micro- 
scope, and it is unreasonable to expect to see from the first all that 
an expert sees. 

2. The patient should be placed at least three feet from the 
tube, else there is likely to be distortion and magnification of the 
shadows corresponding to the organs examined. The tube should 
be placed at such a height as to be opposite the most important 
object to be examined, and always in the median line. 

3. Patients may be examined either in the upright position — 
the tube about three feet from the patient's back — the fluoroscope 
resting against the chest — or in the recumbent position, supported 
on a canvas cot with the tube underneath. I prefer the upright 
position. The patient's arms should always be extended forward 
so as to get the scapulae out of the way. 

4. To concentrate the light upon a spot of special interest, we 
.may use a metal plate with a rectangular opening about two by 
three inches near one end. When this plate is held between the 
tube and the patient, so that the opening is opposite the spot to 
be examined, the rays pass through the opening, but are intercepted 
by the metal around it. The hand which holds this plate should 
be protected from the action of the rays. 



300 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

5. To mark on the chest the outlines of the shadows seen with 
the fluoroscope, a pencil enclosed in a tube of brass is useful ; the 
brass jacket makes the pencil visible and enables us to adjust its 
point to the outlines on the chest. An ordinary pencil is pene- 
trated by the rays completely, and it is hard to draw with a pencil 
which we cannot see. 

II. The Normal Fluoroscopic Picture (see Fig. 138). 

The lungs appear as the lightest part of the field owing to the 
large amount of air they contain ; at the end of full inspiration, 
they become still lighter. Against the light lung areas, the out- 
lines of the ribs and of the vertebral column (with the sternum super- 
imposed) are clearly visible. Less clear, but usually quite distin- 
guishable, are the outlines of the heart and the upper border of the 
liver. A slight shadow (see Fig. 139) is often noticed just to the 
right and to the left of the heart in a position corresponding to the 
larger bronchi. The spleen is not usually to be made out clearly, 
but the upper surface of the diaphragm above it is generally visible. 
The contractions of the heart and the movements of the diaphragm 
are usually clear, and any restriction of the respiratory excursion 
on one side can be noted, though the fluoroscope has no advantages 
over the inspection of Litten's diaphragm shadow (see p. 23) for 
this purpose. 

Abrams has noted that if the skin of the precordia is irritated 
by cold or pain, a reduction in the size of the heart occurs ("heart 
reflex ") for a few seconds. 

In children all these phenomena are especially clear, owing to 
the thinness of their chest walls and we note at once how much 
more horizontal the child's heart is than the adult's (see Fig. 138). 

III. The Fluoroscope in Disease. 

I shall mention first those diseases in which the fluoroscope fur- 
nishes us the most valuable information. 

1. Aneurism. — Small aneurisms of the transverse or descending 
aorta may sometimes be recognized by the se-rays when no other 



RADIOSCOPY OF THE CHEST. 



301 






Chest of Healthy Boy aged 
nine years. 



Incipient Phthisis at Right Chest of Healthy Adult. 

Apex. 






Advanced Phthisis (cavity?). Advanced Phthisis. Bilateral Phthisis at Apices. 






Advanced Phthisis. 



Advanced Phthisis. 



Pulmonary Emphysema. 



n 




Aortic Aneurism. Aneurism of Left Auricle. Fibroid Phthisis of Right Lung. 

Heart drawn to the right. 

Fig. 138.— Twelve Radiographs of the Chest, as Seen from Behind (after Walsham). 



302 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

method of physical examination yields satisfactory evidence. An 
abnormal shadow appears at one side of the sternum (see Fig. 140) 
and may sometimes be seen to pulsate. |In other cases the fluoro- 
scopic evidence is not the only evidence, but tends to confirm or 




Fig. 139.— Radiograph of a Case of Transposition of the Viscera. (After Gibson.) 

dispel suspicions aroused by the ordinary methods of examination. 

Aneurism of the heart itself is recognizable, according to F. H. 
Williams, by the fluoroscopic examination. No other method of 
examination gives us any evidence of such a lesion. 

2. Determination of the Cardiac Outlines in Patients with Em- 
physema and Fat Chest Walls. — Emphysema spoils cardiac percus- 



RADIOSCOPY OF THE CHEST. 



303 



sion and interferes with inspection and palpation. Bnt in fluoro- 
scopic work emphysema is a boon and a blessing, for it renders the 
cardiac outlines more distinct than usual. Hence, for determining 
the size and position of the heart in such cases, the arrays give 
genuine assistance, as they also do when mapping out the heart in 
women with large breasts and fat chest walls. 

3. Central Pneumonia. — Williams and others have succeeded 




Aneurismal sac. 



Heart. 



Fig. 140.— Front View of Thoracic Aneurism. The heart displaced downward. 



in identifying foci of solidification beneath the surface of the lungs 
when no other physical signs could be obtained. It must be re- 
membered, however, that congestion of the lung, oedema, atelec- 
tasis, and pleural thickening produce shadows similar to those of 
solidified lung. 

4. Tuberculosis. — It is still a matter of doubt whether tubercu- 
lous foci can be recognized by the fluoroscope before the disease has 



304 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

progressed sufficiently to produce localized rales, diminished breath 
sounds, or restriction of Littems phrenic phenomenon. 

Slight opacities have been noted in cases which later turned out 
to be tuberculosis, and which had not previously been diagnosed, 
but the shadows perceived by the fluoroscope are capable of many 
interpretations and correspond (as above said) to various pathologi- 
cal conditions. Old quiescent foci may appear like advancing le- 



Aneurismal sac. 



Heart. 




Fig. 141.— Aneurismal Sac Radiographed from Behind. 

sions and thus lead to serious errors. TVe do not want to hurry a 
patient off to Colorado or Davos on account of the shadow thrown 
by a long-healed lesion. Further, in some cases of rheumatism, 
ansemia, debility, and convalescent typhoid, appearances very simi- 
lar to those of tuberculosis may be found (Williams). Hence the 
intrepretation of slight lung shadows in cases of suspected incipient 
phthisis is by no means easy. 



RADIOSCOPY OF THE CHEST. 305 

Advanced phthisis renders the lungs relatively opaque to the 
Roentgen rays except where extensive excavation has occurred; 
here we see a light area in a dark background (see Fig. 138). 

Xo satisfactory radiographs of cases of incipient phthisis have 
so far been published, so far as I am aware. 

5. Pleuritic Effusions. — The displacement of the heart is some- 
times better shown by the arrays than by ordinary methods of ex- 
amination, since the compensatory hypertrophy of the sound lung, 
which interferes with percussion and palpation of the heart, renders 
radioscopy easier. 

The fluid exudate intercepts the rays perceptibly, and when the 
movements of the diaphragm are not abolished on the affected side, 
the line corresponding to the surface of the fluid can be seen to 
move up and down with respiration. 

Small fluid accumulations flatten the normal curve of the upper 
surface of the diaphragm by filling up the chink between the inner 
surface of the chest in the axilla and the line of the diaphragm at 
that point. 

6. Emphysema. — The lungs become unusually transparent and 
owing to the low pocition of the diaphragm the heart descends and 
assumes a very vertical position ("ptosis of the heart"); these 
points are very clearly seen with the fluoroscope. 

Radiographs. 

But little use has thus far been made of radiographs in study- 
ing diseases of the chest. The movements of the heart, of the 
chest walls, and of the diaphragm render all the outlines indistinct. 
For aneurisms, especially those containing a thick layer of clot, and 
for intrathoracic tumors, radiographs may be very useful, and 
bronchial lymph glands are sometimes rendered visible. 
20 



306 PHYSICAL DIAGNOSIS OF DISEASES OF THE CHEST. 

APPENDIX E. 
THE SPHYGMOGRAPH. 

This instrument consists of a system of levers by means of which 
the pulsations of the radial artery are transferred to a needle whose 
oscillations can be graphically recorded upon a piece of smoked pa- 
per. It is a very fascinating little toy, but in its present form is 
almost devoid of practical usefulness owing to the impossibility of 
eliminating the personal equation when using it. The size and, to 
a certain extent, the shape of the wave traced upon the smoked 
paper can be influenced at will by the amount of pressure with 
which the instrument is applied to the wrist. If an instrument is 
applied with a pressure of three ounces to the wrist of A, and then 
with the same pressure to the wrist of B, the force exerted upon 
the artery may be quite different in the two cases owing to the dif- 
ferent shape of the wrist in the two individuals. 

Almost any type of tracing can be obtained from a normal pulse 
by varying the pressure. 

This objection is fatal to the use of the sphygmograph as an in- 
strument of precision, and although it is capable of recording tiny 
secondary waves impalpable by the fingers, it has yet to be shown 
that it reveals anything of practical diagnostic value which is not 
appreciated by skilled fingers. For these reasons I have given no 
account of the instrument in the body of this work. 



INDEX. 



Abrams, 76, 105, 292 

Abscess, pulmonary, 290 

Adenitis, 41 

Amphoric breathing, 103 

Anatomy, 2 

Aneurism, 220-229, 293 

Aortic aneurism, 33, 220-229 

disease, 170-187 

regurgitation, 170 

roughening, 184 

second sound, 121 

stenosis, 181 
Apex, cardiac, displacement of, 29 

position of, 26 

retraction, 31 
Arrhythmia, 161, 204 
Arterial movements, 36 

murmurs, 140 

sounds, 124 

wall, condition of, 55 
Asthma, 261, 263 
Atelectasis, 104, 292 " 
Auscultation, 77-141 

mediate and immediate, 78 

of the heart, 113-141 

of the lungs, 91-112 " 

Barrel chest, 9 

Bradycardia, 51, 203 

Breathing (see Respiration), 16, 21, 

23, 92 
Broadbent, 161, 217 



Bronchial (see Tubular) 

breathing, 95, 102, 239, 280 
Bronchiectasis, 264 
Bronchitis, 233, 245' 

Cancer of lung, 291 
Capillary pulse, 38, 172 
Cardiac (see Heart) 
impulse, 23, 42 

displacement of, 29, 281 

character of, 148 
Cirrhosis of the lung, 265 
Compensation, establishment and 

failure of, 144 
Congenital heart disease, 206 
Cough, effect of, 107, 245 
Curvature, spinal, 14 
Cyanosis, 39 

Deformities, 14 
Diaphragm, movements of, 23 
Diastolic murmur, 137, 181, 192 

shock, 222 

sound, 164, 225 
Dilatation, cardiac, 146, 199 
Ductus arteriosus, persistence of, 207 
Dyspnoea, 18 

Egophony, 111 
Emphysema, 258 

complementary, 262 

interstitial, 262 

large-lunged, 258 



308 



INDEX. 



Emphysema, senile, 258 

with bronchitis, 261 
Empyema, 283, 28-4 
Endocarditis, acute, 296 

chronic, 151 
Epigastric pulsation, 82 
Expansion, 16 

diminished, 17 

increased, 18 

Eattt degeneration, 201 

overgrowth, 201 
Flattening of the chest, 14 
Eoramen ovale, patency of, 207 
Fremitus, tactile, 44 

vocal, 109 
Friction, pleural, 107, 271 

pericardial, 209 

Gangrene of lungs, 290 
Glands, 41 

ILemic murmurs, 136 
Heart (see also Cardiac), 141 
aneurism of, 301 
dilatation of, 146 
diseases of, 141-205 
hypertrophy of, 146 
murmurs, 126 

sounds, accentuation of, 120 
doubling of, 118 
metallic, 124 
muffled, 124 
rhythm of, 123 
shortening of, 117 
Hydropericardium, 219 
Hydrothorax, 266 

Hypertrophy, cardiac, signs of, 146 
Hypostatic congestion of lung, 293 

Infants, examination of, 297 
Jaundice, 40 



Litten, 23 
Lung reflex, 76 
Lungs, abscess of, 290 

cancer of, 291 

diseases of, 233-293 

emphysema of, 258 

fistula-sound, 112 

gangrene of. 290 

oedema of, 293 

Mediastinal tuberculosis, 296 

tumors, 293 
Mediastinitis, 216, 295 
Mediastinum, diseases of, 293 
Metallic heart sounds, 124 

tinkle, 112 
Mitral valve, diseases of, 151-170 

insufficiency of, 151 

stenosis of, 161 
Murmurs, arterial, 140 

cardiac, 126-140 

cardio-respiratory, 138 

functional or haemic, 136 

venous, 139 
Muscle-sounds, 84 
Myocarditis, acute, 199 

chronic, 201 

Neuroses, cardiac, 202 
(Edema, 235, 293 

Pallor, 40 

Palpation, 42 

Palpitation, 205 

Paralytic chest, 8 

Parietal disease (see Myocarditis), 198 

Percussion, 58 

auscultatory, 65 

immediate, 58 

mediate. 58 

palpatory, 67 

resonance, 67 



INDEX. 



309 



Percussion resonance, amphoric, 75 
cracked-pot, 74 
diminished, 69 
tympanitic, 70 
vesicular, 68 

technique of, 58 
Pericardium, diseases of, 209, 219 
Pericarditis, 209 

adhesive, 32, 216 

plastic, 209 

with effusion, 212 
Phthisis, 252 
Pleural thickening, 283 
Pleurisy, 271-284 

encapsulated, 283 

plastic, 271 

pulsating, 284 

with effusion, 273 
Pneumonia, croupous, 237 

inhalation, 244 
Pneumohydrothorax, 268 
Pneumothorax, 111, 266 
Pulmonary abscess, 290 

atelectasis, 104, 292 

emphysema, 258 

gangrene, 290 

oedema, 293 

regurgitation, 192 

stenosis, 193 

tuberculosis, 245 

tympanites, 262 
Pulmonic second sound, 120 
Pulsation, abnormal, 48 
Pulse, 49 

capillary, 173 

compressibility of, 52 

Corrigan's, 172 

dicrotic, 52 

rate, 51 

rhythm, 51 

tension, 53 

wave, size and shape of, 52 



Rachitis, effects on the thorax, 7 
Radioscopy, 227, 298 
Rales, 103 

bilateral, 234 

crepitant, 105 

dry, 104 

moist, 104 

musical, 106 

palpable, 47 

subcrepitant, 105 

unilateral, 245 
Resistance, sense of, 76 
Resonance (see Percussion), 67 
Respiration, amphoric, 98 

asthmatic, 21, 97, 263 

bronchial or tubular, 95 

broncho-vesicular, 96 

Cheyne-Stokes, 22 

cogwheel, 98 

diminished, 100, 279 

emphysematous, 97 

exaggerated, 99, 266, 279 

metamorphosing, 98 

normal, 68 

restrained, 22 

shallow, 23 

stridulous, 23 

types of, 92 

vesicular, 93 
Rhythm, cardiac, 123, 165 

modifications of, 123, 165 

respiratory, 21 

Sphygmograph, 235 

Stethoscope, choice of, 78 

use of, 83 
Succussion, 111 
Syphilis of the lung, 264 



Tachycardia, 202 
Tactile fremitus 
44 



(see Fremitus) , 



310 



INDEX. 



Tension of the pulse, 53 
Thrills, 43 

in aneurism, 222 

in aortic stenosis, 184 

in congenital heart disease, 206, 
208 

in mitral stenosis, 164 
Tracheal tug, 223 
Tracheitis, 233 
Tricuspid regurgitation, 187 

stenosis, 191 
Tuberculosis, advanced, 249 

incipient, 245 

pulmonary, 244 



Tumors, 15, 48, 221, 291, 293 

Valve areas, 113 

lesions, 151-197 
Valvular disease, 141, 151-197 

heart sounds, 117, 199, 202 
Venous murmur, 139 

pulsations, 35, 188 

sound, 125 
Ventricle, left, hypertrophy of, 147 

right, hypertrophy of, 148 
Ventricular septum, defects in, 207 
Voice sounds, spoken, 110 

whispered, 109, 238 






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